Skip to main content
Erschienen in: Neurotherapeutics 4/2020

01.10.2020 | Current Perspectives

The Pharmacogenetics of Rituximab: Potential Implications for Anti-CD20 Therapies in Multiple Sclerosis

verfasst von: Michael Zhong, Anneke van der Walt, Maria Pia Campagna, Jim Stankovich, Helmut Butzkueven, Vilija Jokubaitis

Erschienen in: Neurotherapeutics | Ausgabe 4/2020

Einloggen, um Zugang zu erhalten

Abstract

There are a broad range of disease-modifying therapies (DMTs) available in relapsing-remitting multiple sclerosis (RRMS), but limited biomarkers exist to personalise DMT choice. All DMTs, including monoclonal antibodies such as rituximab and ocrelizumab, are effective in preventing relapses and preserving neurological function in MS. However, each agent harbours its own risk of therapeutic failure or adverse events. Pharmacogenetics, the study of the effects of genetic variation on therapeutic response or adverse events, could improve the precision of DMT selection. Pharmacogenetic studies of rituximab in MS patients are lacking, but pharmacogenetic markers in other rituximab-treated autoimmune conditions have been identified. This review will outline the wider implications of pharmacogenetics and the mechanisms of anti-CD20 agents in MS. We explore the non-MS rituximab literature to characterise pharmacogenetic variants that could be of prognostic relevance in those receiving rituximab, ocrelizumab or other monoclonal antibodies for MS.
Anhänge
Nur mit Berechtigung zugänglich
Literatur
1.
Zurück zum Zitat Jokubaitis VG, Spelman T, Kalincik T, et al. Predictors of disability worsening in clinically isolated syndrome. Annals of Clinical and Translational Neurology. 2015;2:479–491.PubMedPubMedCentralCrossRef Jokubaitis VG, Spelman T, Kalincik T, et al. Predictors of disability worsening in clinically isolated syndrome. Annals of Clinical and Translational Neurology. 2015;2:479–491.PubMedPubMedCentralCrossRef
2.
Zurück zum Zitat Jokubaitis VG, Spelman T, Kalincik T, et al. Predictors of long-term disability accrual in relapse-onset multiple sclerosis: Predictors of MS Outcomes. Annals of Neurology. 2016;80:89–100.PubMedCrossRef Jokubaitis VG, Spelman T, Kalincik T, et al. Predictors of long-term disability accrual in relapse-onset multiple sclerosis: Predictors of MS Outcomes. Annals of Neurology. 2016;80:89–100.PubMedCrossRef
3.
Zurück zum Zitat Kalincik T, Manouchehrinia A, Sobisek L, et al. Towards personalized therapy for multiple sclerosis: prediction of individual treatment response. Brain. 2017;140:2426–2443.PubMedCrossRef Kalincik T, Manouchehrinia A, Sobisek L, et al. Towards personalized therapy for multiple sclerosis: prediction of individual treatment response. Brain. 2017;140:2426–2443.PubMedCrossRef
5.
Zurück zum Zitat Roden DM, McLeod HL, Relling MV, et al. Pharmacogenomics. The Lancet. 2019;394:521–532.CrossRef Roden DM, McLeod HL, Relling MV, et al. Pharmacogenomics. The Lancet. 2019;394:521–532.CrossRef
7.
Zurück zum Zitat Peterson JF, Roden DM, Orlando LA, et al. Building evidence and measuring clinical outcomes for genomic medicine. The Lancet. 2019;394:604–610.CrossRef Peterson JF, Roden DM, Orlando LA, et al. Building evidence and measuring clinical outcomes for genomic medicine. The Lancet. 2019;394:604–610.CrossRef
8.
Zurück zum Zitat Telenti A, Pierce LCT, Biggs WH, et al. Deep sequencing of 10,000 human genomes. Proc Natl Acad Sci USA. 2016;113:11901–11906.PubMedCrossRef Telenti A, Pierce LCT, Biggs WH, et al. Deep sequencing of 10,000 human genomes. Proc Natl Acad Sci USA. 2016;113:11901–11906.PubMedCrossRef
9.
Zurück zum Zitat Scott RH, Fowler TA, Caulfield M. Genomic medicine: time for health-care transformation. The Lancet. 2019;394:454–456.CrossRef Scott RH, Fowler TA, Caulfield M. Genomic medicine: time for health-care transformation. The Lancet. 2019;394:454–456.CrossRef
11.
Zurück zum Zitat Van Driest S, Shi Y, Bowton E, et al. Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing. Clin Pharmacol Ther. 2014;95:423–431.PubMedCrossRef Van Driest S, Shi Y, Bowton E, et al. Clinically Actionable Genotypes Among 10,000 Patients With Preemptive Pharmacogenomic Testing. Clin Pharmacol Ther. 2014;95:423–431.PubMedCrossRef
12.
Zurück zum Zitat Ji Y, Skierka JM, Blommel JH, et al. Preemptive Pharmacogenomic Testing for Precision Medicine. The Journal of Molecular Diagnostics. 2016;18:438–445.PubMedCrossRef Ji Y, Skierka JM, Blommel JH, et al. Preemptive Pharmacogenomic Testing for Precision Medicine. The Journal of Molecular Diagnostics. 2016;18:438–445.PubMedCrossRef
13.
Zurück zum Zitat Dinama O, Warren AM, Kulkarni J. The role of pharmacogenomic testing in psychiatry: Real world examples. Australian & New Zealand Journal of Psychiatry. 2014;48:778–778.CrossRef Dinama O, Warren AM, Kulkarni J. The role of pharmacogenomic testing in psychiatry: Real world examples. Australian & New Zealand Journal of Psychiatry. 2014;48:778–778.CrossRef
14.
Zurück zum Zitat Hicks J, Bishop J, Sangkuhl K, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors. Clin Pharmacol Ther. 2015;98:127–134.PubMedPubMedCentralCrossRef Hicks J, Bishop J, Sangkuhl K, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors. Clin Pharmacol Ther. 2015;98:127–134.PubMedPubMedCentralCrossRef
15.
Zurück zum Zitat Hicks JK, Stowe D, Willner MA, et al. Implementation of Clinical Pharmacogenomics within a Large Health System: From Electronic Health Record Decision Support to Consultation Services. Pharmacotherapy. 2016;36:940–948.PubMedCrossRef Hicks JK, Stowe D, Willner MA, et al. Implementation of Clinical Pharmacogenomics within a Large Health System: From Electronic Health Record Decision Support to Consultation Services. Pharmacotherapy. 2016;36:940–948.PubMedCrossRef
16.
Zurück zum Zitat Crews KR, Gaedigk A, Dunnenberger HM, et al. Clinical Pharmacogenetics Implementation Consortium Guidelines for Cytochrome P450 2D6 Genotype and Codeine Therapy: 2014 Update. Clin Pharmacol Ther. 2014;95:376–382.PubMedPubMedCentralCrossRef Crews KR, Gaedigk A, Dunnenberger HM, et al. Clinical Pharmacogenetics Implementation Consortium Guidelines for Cytochrome P450 2D6 Genotype and Codeine Therapy: 2014 Update. Clin Pharmacol Ther. 2014;95:376–382.PubMedPubMedCentralCrossRef
17.
Zurück zum Zitat Bertilsson L, Dahl M-L, Dalén P, et al. Molecular genetics of CYP2D6: clinical relevance with focus on psychotropic drugs. Br J Clin Pharmacol. 2002;53:111–122.PubMedPubMedCentralCrossRef Bertilsson L, Dahl M-L, Dalén P, et al. Molecular genetics of CYP2D6: clinical relevance with focus on psychotropic drugs. Br J Clin Pharmacol. 2002;53:111–122.PubMedPubMedCentralCrossRef
18.
Zurück zum Zitat Cavallari LH, Johnson JA. A case for genotype-guided pain management. Pharmacogenomics. 2019;20:705–708.PubMedCrossRef Cavallari LH, Johnson JA. A case for genotype-guided pain management. Pharmacogenomics. 2019;20:705–708.PubMedCrossRef
19.
Zurück zum Zitat Gasche Y, Daali Y, Fathi M, et al. Codeine intoxication associated with ultrarapid CYP2D6 metabolism. N Engl J Med. 2004;351:2827–2831.PubMedCrossRef Gasche Y, Daali Y, Fathi M, et al. Codeine intoxication associated with ultrarapid CYP2D6 metabolism. N Engl J Med. 2004;351:2827–2831.PubMedCrossRef
20.
Zurück zum Zitat Mega JL, Simon T, Collet J-P, et al. Reduced-function CYP2C19 genotype and risk of adverse clinical outcomes among patients treated with clopidogrel predominantly for PCI: a meta-analysis. JAMA. 2010;304:1821–1830.PubMedPubMedCentralCrossRef Mega JL, Simon T, Collet J-P, et al. Reduced-function CYP2C19 genotype and risk of adverse clinical outcomes among patients treated with clopidogrel predominantly for PCI: a meta-analysis. JAMA. 2010;304:1821–1830.PubMedPubMedCentralCrossRef
21.
Zurück zum Zitat Notarangelo FM, Maglietta G, Bevilacqua P, et al. Pharmacogenomic Approach to Selecting Antiplatelet Therapy in Patients With Acute Coronary Syndromes: The PHARMCLO Trial. J Am Coll Cardiol. 2018;71:1869–1877.PubMedCrossRef Notarangelo FM, Maglietta G, Bevilacqua P, et al. Pharmacogenomic Approach to Selecting Antiplatelet Therapy in Patients With Acute Coronary Syndromes: The PHARMCLO Trial. J Am Coll Cardiol. 2018;71:1869–1877.PubMedCrossRef
22.
Zurück zum Zitat Cavallari LH, Lee CR, Beitelshees AL, et al. Multisite Investigation of Outcomes With Implementation of CYP2C19 Genotype-Guided Antiplatelet Therapy After Percutaneous Coronary Intervention. JACC: Cardiovascular Interventions. 2018;11:181–191.PubMed Cavallari LH, Lee CR, Beitelshees AL, et al. Multisite Investigation of Outcomes With Implementation of CYP2C19 Genotype-Guided Antiplatelet Therapy After Percutaneous Coronary Intervention. JACC: Cardiovascular Interventions. 2018;11:181–191.PubMed
23.
Zurück zum Zitat Ozawa T, Suda M, Ikegami R, et al. Dual Antiplatelet Therapy Guided by CYP2C19 Polymorphisms after Implantation of Second-Generation Drug-Eluting Stents for Management of Acute Coronary Syndrome. Int Heart J. 2018;59:21–26.PubMedCrossRef Ozawa T, Suda M, Ikegami R, et al. Dual Antiplatelet Therapy Guided by CYP2C19 Polymorphisms after Implantation of Second-Generation Drug-Eluting Stents for Management of Acute Coronary Syndrome. Int Heart J. 2018;59:21–26.PubMedCrossRef
24.
Zurück zum Zitat Joo HJ, Ahn SG, Park JH, et al. Effects of genetic variants on platelet reactivity and one-year clinical outcomes after percutaneous coronary intervention: A prospective multicentre registry study. Sci Rep. 2018;8:1229.PubMedPubMedCentralCrossRef Joo HJ, Ahn SG, Park JH, et al. Effects of genetic variants on platelet reactivity and one-year clinical outcomes after percutaneous coronary intervention: A prospective multicentre registry study. Sci Rep. 2018;8:1229.PubMedPubMedCentralCrossRef
26.
Zurück zum Zitat Edwards JCW, Szczepanski L, Szechinski J, et al. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med. 2004;350:2572–2581.PubMedCrossRef Edwards JCW, Szczepanski L, Szechinski J, et al. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med. 2004;350:2572–2581.PubMedCrossRef
27.
Zurück zum Zitat Hauser SL, Waubant E, Arnold DL, et al. B-cell depletion with rituximab in relapsing-remitting multiple sclerosis. N Engl J Med. 2008;358:676–688.PubMedCrossRef Hauser SL, Waubant E, Arnold DL, et al. B-cell depletion with rituximab in relapsing-remitting multiple sclerosis. N Engl J Med. 2008;358:676–688.PubMedCrossRef
28.
29.
Zurück zum Zitat Baecher-Allan C, Kaskow BJ, Weiner HL. Multiple Sclerosis: Mechanisms and Immunotherapy. Neuron. 2018;97:742–768.PubMedCrossRef Baecher-Allan C, Kaskow BJ, Weiner HL. Multiple Sclerosis: Mechanisms and Immunotherapy. Neuron. 2018;97:742–768.PubMedCrossRef
30.
Zurück zum Zitat Gresle MM, Jordan MA, Stankovich J, et al. Multiple sclerosis risk variants regulate gene expression in innate and adaptive immune cells. Life Science Alliance. 2020;3:e202000650.PubMedPubMedCentralCrossRef Gresle MM, Jordan MA, Stankovich J, et al. Multiple sclerosis risk variants regulate gene expression in innate and adaptive immune cells. Life Science Alliance. 2020;3:e202000650.PubMedPubMedCentralCrossRef
31.
Zurück zum Zitat Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. Nat Rev Immunol. 2015;15:545–558.PubMedCrossRef Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. Nat Rev Immunol. 2015;15:545–558.PubMedCrossRef
32.
Zurück zum Zitat Sabatino JJ, Pröbstel A-K, Zamvil SS. B cells in autoimmune and neurodegenerative central nervous system diseases. Nature Reviews Neuroscience. 2019;20:728–745.PubMedCrossRef Sabatino JJ, Pröbstel A-K, Zamvil SS. B cells in autoimmune and neurodegenerative central nervous system diseases. Nature Reviews Neuroscience. 2019;20:728–745.PubMedCrossRef
33.
Zurück zum Zitat Wanleenuwat P, Iwanowski P. Role of B cells and antibodies in multiple sclerosis. Multiple Sclerosis and Related Disorders. 2019;36:101416.PubMedCrossRef Wanleenuwat P, Iwanowski P. Role of B cells and antibodies in multiple sclerosis. Multiple Sclerosis and Related Disorders. 2019;36:101416.PubMedCrossRef
34.
Zurück zum Zitat Breij ECW, Brink BP, Veerhuis R, et al. Homogeneity of active demyelinating lesions in established multiple sclerosis. Ann Neurol. 2008;63:16–25.PubMedCrossRef Breij ECW, Brink BP, Veerhuis R, et al. Homogeneity of active demyelinating lesions in established multiple sclerosis. Ann Neurol. 2008;63:16–25.PubMedCrossRef
35.
Zurück zum Zitat Prineas JW, Wright RG. Macrophages, lymphocytes, and plasma cells in the perivascular compartment in chronic multiple sclerosis. Lab Invest. 1978;38:409–421.PubMed Prineas JW, Wright RG. Macrophages, lymphocytes, and plasma cells in the perivascular compartment in chronic multiple sclerosis. Lab Invest. 1978;38:409–421.PubMed
36.
Zurück zum Zitat Qin Y, Duquette P, Zhang Y, et al. Clonal expansion and somatic hypermutation of V(H) genes of B cells from cerebrospinal fluid in multiple sclerosis. J Clin Invest. 1998;102:1045–1050.PubMedPubMedCentralCrossRef Qin Y, Duquette P, Zhang Y, et al. Clonal expansion and somatic hypermutation of V(H) genes of B cells from cerebrospinal fluid in multiple sclerosis. J Clin Invest. 1998;102:1045–1050.PubMedPubMedCentralCrossRef
37.
Zurück zum Zitat Qin Y, Duquette P, Zhang Y, et al. Intrathecal B-Cell Clonal Expansion, an Early Sign of Humoral Immunity, in the Cerebrospinal Fluid of Patients with Clinically Isolated Syndrome Suggestive of Multiple Sclerosis. Lab Invest. 2003;83:1081–1088.PubMedCrossRef Qin Y, Duquette P, Zhang Y, et al. Intrathecal B-Cell Clonal Expansion, an Early Sign of Humoral Immunity, in the Cerebrospinal Fluid of Patients with Clinically Isolated Syndrome Suggestive of Multiple Sclerosis. Lab Invest. 2003;83:1081–1088.PubMedCrossRef
38.
Zurück zum Zitat Obermeier B, Mentele R, Malotka J, et al. Matching of oligoclonal immunoglobulin transcriptomes and proteomes of cerebrospinal fluid in multiple sclerosis. Nat Med. 2008;14:688–693.PubMedCrossRef Obermeier B, Mentele R, Malotka J, et al. Matching of oligoclonal immunoglobulin transcriptomes and proteomes of cerebrospinal fluid in multiple sclerosis. Nat Med. 2008;14:688–693.PubMedCrossRef
39.
Zurück zum Zitat DiLillo DJ, Hamaguchi Y, Ueda Y, et al. Maintenance of long-lived plasma cells and serological memory despite mature and memory B cell depletion during CD20 immunotherapy in mice. J Immunol. 2008;180:361–371.PubMedCrossRef DiLillo DJ, Hamaguchi Y, Ueda Y, et al. Maintenance of long-lived plasma cells and serological memory despite mature and memory B cell depletion during CD20 immunotherapy in mice. J Immunol. 2008;180:361–371.PubMedCrossRef
40.
Zurück zum Zitat Greenfield AL, Hauser SL. B-cell Therapy for Multiple Sclerosis: Entering an era: MS: Entering the Era of B-Cell Therapy. Ann Neurol. 2018;83:13–26.PubMedPubMedCentralCrossRef Greenfield AL, Hauser SL. B-cell Therapy for Multiple Sclerosis: Entering an era: MS: Entering the Era of B-Cell Therapy. Ann Neurol. 2018;83:13–26.PubMedPubMedCentralCrossRef
41.
Zurück zum Zitat Mathias A, Perriard G, Canales M, et al. Increased ex vivo antigen presentation profile of B cells in multiple sclerosis. Mult Scler. 2017;23:802–809.PubMedCrossRef Mathias A, Perriard G, Canales M, et al. Increased ex vivo antigen presentation profile of B cells in multiple sclerosis. Mult Scler. 2017;23:802–809.PubMedCrossRef
42.
Zurück zum Zitat Jelcic I, Al Nimer F, Wang J, et al. Memory B Cells Activate Brain-Homing, Autoreactive CD4+ T Cells in Multiple Sclerosis. Cell. 2018;175:85-100.e23.PubMedPubMedCentralCrossRef Jelcic I, Al Nimer F, Wang J, et al. Memory B Cells Activate Brain-Homing, Autoreactive CD4+ T Cells in Multiple Sclerosis. Cell. 2018;175:85-100.e23.PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Duddy M, Niino M, Adatia F, et al. Distinct Effector Cytokine Profiles of Memory and Naive Human B Cell Subsets and Implication in Multiple Sclerosis. J Immunol. 2007;178:6092–6099.PubMedCrossRef Duddy M, Niino M, Adatia F, et al. Distinct Effector Cytokine Profiles of Memory and Naive Human B Cell Subsets and Implication in Multiple Sclerosis. J Immunol. 2007;178:6092–6099.PubMedCrossRef
45.
Zurück zum Zitat Bar-Or A, Fawaz L, Fan B, et al. Abnormal B-cell cytokine responses a trigger of T-cell-mediated disease in MS? Ann Neurol. 2010;67:452–461.PubMedCrossRef Bar-Or A, Fawaz L, Fan B, et al. Abnormal B-cell cytokine responses a trigger of T-cell-mediated disease in MS? Ann Neurol. 2010;67:452–461.PubMedCrossRef
46.
Zurück zum Zitat Korn T, Mitsdoerffer M, Croxford AL, et al. IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+ regulatory T cells. Proceedings of the National Academy of Sciences. 2008;105:18460–18465.CrossRef Korn T, Mitsdoerffer M, Croxford AL, et al. IL-6 controls Th17 immunity in vivo by inhibiting the conversion of conventional T cells into Foxp3+ regulatory T cells. Proceedings of the National Academy of Sciences. 2008;105:18460–18465.CrossRef
47.
Zurück zum Zitat Molnarfi N, Schulze-Topphoff U, Weber MS, et al. MHC class II-dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies. J Exp Med. 2013;210:2921–2937.PubMedPubMedCentralCrossRef Molnarfi N, Schulze-Topphoff U, Weber MS, et al. MHC class II-dependent B cell APC function is required for induction of CNS autoimmunity independent of myelin-specific antibodies. J Exp Med. 2013;210:2921–2937.PubMedPubMedCentralCrossRef
48.
Zurück zum Zitat Barr TA, Shen P, Brown S, et al. B cell depletion therapy ameliorates autoimmune disease through ablation of IL-6–producing B cells. The Journal of Experimental Medicine. 2012;209:1001–1010.PubMedPubMedCentralCrossRef Barr TA, Shen P, Brown S, et al. B cell depletion therapy ameliorates autoimmune disease through ablation of IL-6–producing B cells. The Journal of Experimental Medicine. 2012;209:1001–1010.PubMedPubMedCentralCrossRef
49.
Zurück zum Zitat Li R, Rezk A, Miyazaki Y, et al. Proinflammatory GM-CSF-producing B cells in multiple sclerosis and B cell depletion therapy. Sci Transl Med. 2015;7:310ra166.PubMedCrossRef Li R, Rezk A, Miyazaki Y, et al. Proinflammatory GM-CSF-producing B cells in multiple sclerosis and B cell depletion therapy. Sci Transl Med. 2015;7:310ra166.PubMedCrossRef
50.
Zurück zum Zitat Kannel K, Alnek K, Vahter L, et al. Changes in Blood B Cell-Activating Factor (BAFF) Levels in Multiple Sclerosis: A Sign of Treatment Outcome. PLoS ONE. 2015;10:e0143393.PubMedPubMedCentralCrossRef Kannel K, Alnek K, Vahter L, et al. Changes in Blood B Cell-Activating Factor (BAFF) Levels in Multiple Sclerosis: A Sign of Treatment Outcome. PLoS ONE. 2015;10:e0143393.PubMedPubMedCentralCrossRef
51.
Zurück zum Zitat Serafini B, Rosicarelli B, Magliozzi R, et al. Detection of Ectopic B-cell Follicles with Germinal Centers in the Meninges of Patients with Secondary Progressive Multiple Sclerosis. Brain Pathology. 2004;14:164–174.PubMedCrossRef Serafini B, Rosicarelli B, Magliozzi R, et al. Detection of Ectopic B-cell Follicles with Germinal Centers in the Meninges of Patients with Secondary Progressive Multiple Sclerosis. Brain Pathology. 2004;14:164–174.PubMedCrossRef
52.
Zurück zum Zitat Magliozzi R, Howell O, Vora A, et al. Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. Brain. 2006;130:1089–1104.CrossRef Magliozzi R, Howell O, Vora A, et al. Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology. Brain. 2006;130:1089–1104.CrossRef
53.
Zurück zum Zitat Lassmann H. New concepts on progressive multiple sclerosis. Curr Neurol Neurosci Rep. 2007;7:239–244.PubMedCrossRef Lassmann H. New concepts on progressive multiple sclerosis. Curr Neurol Neurosci Rep. 2007;7:239–244.PubMedCrossRef
54.
Zurück zum Zitat Corsiero E, Nerviani A, Bombardieri M, et al. Ectopic Lymphoid Structures: Powerhouse of Autoimmunity. Front Immunol. 2016;7:430.PubMedPubMedCentral Corsiero E, Nerviani A, Bombardieri M, et al. Ectopic Lymphoid Structures: Powerhouse of Autoimmunity. Front Immunol. 2016;7:430.PubMedPubMedCentral
55.
Zurück zum Zitat Thaunat O, Patey N, Gautreau C, et al. B cell survival in intragraft tertiary lymphoid organs after rituximab therapy. Transplantation. 2008;85:1648–1653.PubMedCrossRef Thaunat O, Patey N, Gautreau C, et al. B cell survival in intragraft tertiary lymphoid organs after rituximab therapy. Transplantation. 2008;85:1648–1653.PubMedCrossRef
56.
Zurück zum Zitat Monson NL, Cravens PD, Frohman EM, et al. Effect of Rituximab on the Peripheral Blood and Cerebrospinal Fluid B Cells in Patients With Primary Progressive Multiple Sclerosis. Arch Neurol. 2005;62:258–264.PubMedCrossRef Monson NL, Cravens PD, Frohman EM, et al. Effect of Rituximab on the Peripheral Blood and Cerebrospinal Fluid B Cells in Patients With Primary Progressive Multiple Sclerosis. Arch Neurol. 2005;62:258–264.PubMedCrossRef
57.
Zurück zum Zitat Larouche J-F, Bergeron M, Hampson G, et al. Rituximab Cerebrospinal Fluid Levels in Patients with Primary Central Nervous System Lymphoma Treated with Intravenous High Dose Rituximab. Blood. 2011;118:1644–1644.CrossRef Larouche J-F, Bergeron M, Hampson G, et al. Rituximab Cerebrospinal Fluid Levels in Patients with Primary Central Nervous System Lymphoma Treated with Intravenous High Dose Rituximab. Blood. 2011;118:1644–1644.CrossRef
58.
Zurück zum Zitat Krumbholz M, Derfuss T, Hohlfeld R, et al. B cells and antibodies in multiple sclerosis pathogenesis and therapy. Nature Reviews Neurology. 2012;8:613–623.PubMedCrossRef Krumbholz M, Derfuss T, Hohlfeld R, et al. B cells and antibodies in multiple sclerosis pathogenesis and therapy. Nature Reviews Neurology. 2012;8:613–623.PubMedCrossRef
59.
Zurück zum Zitat Leandro MJ. B-cell subpopulations in humans and their differential susceptibility to depletion with anti-CD20 monoclonal antibodies. Arthritis Res Ther. 2013;15 Suppl 1:S3.PubMedPubMedCentralCrossRef Leandro MJ. B-cell subpopulations in humans and their differential susceptibility to depletion with anti-CD20 monoclonal antibodies. Arthritis Res Ther. 2013;15 Suppl 1:S3.PubMedPubMedCentralCrossRef
60.
Zurück zum Zitat Gingele S, Jacobus TL, Konen FF, et al. Ocrelizumab Depletes CD20+ T Cells in Multiple Sclerosis Patients. Cells. 2018;8:12. Gingele S, Jacobus TL, Konen FF, et al. Ocrelizumab Depletes CD20+ T Cells in Multiple Sclerosis Patients. Cells. 2018;8:12.
61.
Zurück zum Zitat Palanichamy A, Jahn S, Nickles D, et al. Rituximab Efficiently Depletes Increased CD20-Expressing T Cells in Multiple Sclerosis Patients. JI. 2014;193:580–586. Palanichamy A, Jahn S, Nickles D, et al. Rituximab Efficiently Depletes Increased CD20-Expressing T Cells in Multiple Sclerosis Patients. JI. 2014;193:580–586.
62.
Zurück zum Zitat Sabatino JJ, Wilson MR, Calabresi PA, et al. Anti-CD20 therapy depletes activated myelin-specific CD8 + T cells in multiple sclerosis. Proc Natl Acad Sci USA. 2019;116:25800–25807.PubMedCrossRef Sabatino JJ, Wilson MR, Calabresi PA, et al. Anti-CD20 therapy depletes activated myelin-specific CD8 + T cells in multiple sclerosis. Proc Natl Acad Sci USA. 2019;116:25800–25807.PubMedCrossRef
64.
Zurück zum Zitat Barkhof F, Kappos L, Wolinsky JS, et al. Onset of clinical and MRI efficacy of ocrelizumab in relapsing multiple sclerosis. Neurology. 2019;93:e1778–e1786.PubMedPubMedCentralCrossRef Barkhof F, Kappos L, Wolinsky JS, et al. Onset of clinical and MRI efficacy of ocrelizumab in relapsing multiple sclerosis. Neurology. 2019;93:e1778–e1786.PubMedPubMedCentralCrossRef
65.
Zurück zum Zitat Roll P, Palanichamy A, Kneitz C, et al. Regeneration of B cell subsets after transient B cell depletion using anti-CD20 antibodies in rheumatoid arthritis. Arthritis Rheum. 2006;54:2377–2386.PubMedCrossRef Roll P, Palanichamy A, Kneitz C, et al. Regeneration of B cell subsets after transient B cell depletion using anti-CD20 antibodies in rheumatoid arthritis. Arthritis Rheum. 2006;54:2377–2386.PubMedCrossRef
66.
Zurück zum Zitat Zhou X, Hu W, Qin X. The Role of Complement in the Mechanism of Action of Rituximab for B-Cell Lymphoma: Implications for Therapy. The Oncologist. 2008;13:954–966.PubMedCrossRef Zhou X, Hu W, Qin X. The Role of Complement in the Mechanism of Action of Rituximab for B-Cell Lymphoma: Implications for Therapy. The Oncologist. 2008;13:954–966.PubMedCrossRef
67.
Zurück zum Zitat Maloney DG. Anti-CD20 Antibody Therapy for B-Cell Lymphomas. N Engl J Med. 2012;366:2008–2016.PubMedCrossRef Maloney DG. Anti-CD20 Antibody Therapy for B-Cell Lymphomas. N Engl J Med. 2012;366:2008–2016.PubMedCrossRef
68.
Zurück zum Zitat Klein C, Lammens A, Schäfer W, et al. Epitope interactions of monoclonal antibodies targeting CD20 and their relationship to functional properties. mAbs. 2013;5:22–33.PubMedPubMedCentralCrossRef Klein C, Lammens A, Schäfer W, et al. Epitope interactions of monoclonal antibodies targeting CD20 and their relationship to functional properties. mAbs. 2013;5:22–33.PubMedPubMedCentralCrossRef
70.
Zurück zum Zitat Yan L, Beckman RA. Pharmacogenetics and pharmacogenomics in oncology therapeutic antibody development. BioTechniques. 2005;39:S565–S568.PubMedCrossRef Yan L, Beckman RA. Pharmacogenetics and pharmacogenomics in oncology therapeutic antibody development. BioTechniques. 2005;39:S565–S568.PubMedCrossRef
71.
Zurück zum Zitat Abuqayyas L, Balthasar JP. Application of knockout mouse models to investigate the influence of FcγR on the tissue distribution and elimination of 8C2, a murine IgG1 monoclonal antibody. Int J Pharm. 2012;439:8–16.PubMedCrossRef Abuqayyas L, Balthasar JP. Application of knockout mouse models to investigate the influence of FcγR on the tissue distribution and elimination of 8C2, a murine IgG1 monoclonal antibody. Int J Pharm. 2012;439:8–16.PubMedCrossRef
72.
Zurück zum Zitat Leipold D, Prabhu S. Pharmacokinetic and Pharmacodynamic Considerations in the Design of Therapeutic Antibodies. Clinical and Translational Science. 2019;12:130–139.PubMedCrossRef Leipold D, Prabhu S. Pharmacokinetic and Pharmacodynamic Considerations in the Design of Therapeutic Antibodies. Clinical and Translational Science. 2019;12:130–139.PubMedCrossRef
73.
Zurück zum Zitat Ryman JT, Meibohm B. Pharmacokinetics of Monoclonal Antibodies: Pharmacokinetics of Monoclonal Antibodies. CPT: Pharmacometrics & Systems Pharmacology. 2017;6:576–588. Ryman JT, Meibohm B. Pharmacokinetics of Monoclonal Antibodies: Pharmacokinetics of Monoclonal Antibodies. CPT: Pharmacometrics & Systems Pharmacology. 2017;6:576–588.
74.
Zurück zum Zitat Glassman PM, Balthasar JP. Mechanistic considerations for the use of monoclonal antibodies for cancer therapy. Cancer Biol Med. 2014;11:20–33.PubMedPubMedCentral Glassman PM, Balthasar JP. Mechanistic considerations for the use of monoclonal antibodies for cancer therapy. Cancer Biol Med. 2014;11:20–33.PubMedPubMedCentral
75.
Zurück zum Zitat Dirks NL, Meibohm B. Population Pharmacokinetics of Therapeutic Monoclonal Antibodies. Clin Pharmacokinet. 2010;49:633–659.PubMedCrossRef Dirks NL, Meibohm B. Population Pharmacokinetics of Therapeutic Monoclonal Antibodies. Clin Pharmacokinet. 2010;49:633–659.PubMedCrossRef
77.
Zurück zum Zitat Kim J, Hayton WL, Robinson JM, et al. Kinetics of FcRn-mediated recycling of IgG and albumin in human: pathophysiology and therapeutic implications using a simplified mechanism-based model. Clin Immunol. 2007;122:146–155.PubMedCrossRef Kim J, Hayton WL, Robinson JM, et al. Kinetics of FcRn-mediated recycling of IgG and albumin in human: pathophysiology and therapeutic implications using a simplified mechanism-based model. Clin Immunol. 2007;122:146–155.PubMedCrossRef
78.
Zurück zum Zitat Hawker K, O’Connor P, Freedman MS, et al. Rituximab in patients with primary progressive multiple sclerosis: Results of a randomized double-blind placebo-controlled multicenter trial. Ann Neurol. 2009;66:460–471.PubMedCrossRef Hawker K, O’Connor P, Freedman MS, et al. Rituximab in patients with primary progressive multiple sclerosis: Results of a randomized double-blind placebo-controlled multicenter trial. Ann Neurol. 2009;66:460–471.PubMedCrossRef
79.
Zurück zum Zitat Berntsson SG, Kristoffersson A, Boström I, et al. Rapidly increasing off-label use of rituximab in multiple sclerosis in Sweden — Outlier or predecessor? Acta Neurologica Scandinavica. 2018;138:327–331.PubMedCrossRef Berntsson SG, Kristoffersson A, Boström I, et al. Rapidly increasing off-label use of rituximab in multiple sclerosis in Sweden — Outlier or predecessor? Acta Neurologica Scandinavica. 2018;138:327–331.PubMedCrossRef
80.
Zurück zum Zitat Naegelin Y, Naegelin P, von Felten S, et al. Association of Rituximab Treatment With Disability Progression Among Patients With Secondary Progressive Multiple Sclerosis. JAMA Neurol. 2019;76:274.PubMedPubMedCentralCrossRef Naegelin Y, Naegelin P, von Felten S, et al. Association of Rituximab Treatment With Disability Progression Among Patients With Secondary Progressive Multiple Sclerosis. JAMA Neurol. 2019;76:274.PubMedPubMedCentralCrossRef
81.
Zurück zum Zitat Collongues N, de Seze J. An update on the evidence for the efficacy and safety of rituximab in the management of neuromyelitis optica. Ther Adv Neurol Disord. 2016;9:180–188.PubMedPubMedCentralCrossRef Collongues N, de Seze J. An update on the evidence for the efficacy and safety of rituximab in the management of neuromyelitis optica. Ther Adv Neurol Disord. 2016;9:180–188.PubMedPubMedCentralCrossRef
82.
Zurück zum Zitat Iorio R, Damato V, Alboini PE, et al. Efficacy and safety of rituximab for myasthenia gravis: a systematic review and meta-analysis. J Neurol. 2015;262:1115–1119.PubMedCrossRef Iorio R, Damato V, Alboini PE, et al. Efficacy and safety of rituximab for myasthenia gravis: a systematic review and meta-analysis. J Neurol. 2015;262:1115–1119.PubMedCrossRef
83.
Zurück zum Zitat Lancaster E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016;12:1–13.PubMedCrossRef Lancaster E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016;12:1–13.PubMedCrossRef
84.
Zurück zum Zitat Winkler U, Jensen M, Manzke O, et al. Cytokine-release syndrome in patients with B-cell chronic lymphocytic leukemia and high lymphocyte counts after treatment with an anti-CD20 monoclonal antibody (rituximab, IDEC-C2B8). Blood. 1999;94:2217–2224.PubMedCrossRef Winkler U, Jensen M, Manzke O, et al. Cytokine-release syndrome in patients with B-cell chronic lymphocytic leukemia and high lymphocyte counts after treatment with an anti-CD20 monoclonal antibody (rituximab, IDEC-C2B8). Blood. 1999;94:2217–2224.PubMedCrossRef
85.
Zurück zum Zitat Barmettler S, Ong M-S, Farmer JR, et al. Association of Immunoglobulin Levels, Infectious Risk, and Mortality With Rituximab and Hypogammaglobulinemia. JAMA Network Open. 2018;1:e184169.PubMedPubMedCentralCrossRef Barmettler S, Ong M-S, Farmer JR, et al. Association of Immunoglobulin Levels, Infectious Risk, and Mortality With Rituximab and Hypogammaglobulinemia. JAMA Network Open. 2018;1:e184169.PubMedPubMedCentralCrossRef
86.
Zurück zum Zitat Roberts DM, Jones RB, Smith RM, et al. Rituximab-associated hypogammaglobulinemia: incidence, predictors and outcomes in patients with multi-system autoimmune disease. J Autoimmun. 2015;57:60–65.PubMedCrossRef Roberts DM, Jones RB, Smith RM, et al. Rituximab-associated hypogammaglobulinemia: incidence, predictors and outcomes in patients with multi-system autoimmune disease. J Autoimmun. 2015;57:60–65.PubMedCrossRef
87.
Zurück zum Zitat Hu Y, Nie H, Yu H-H, et al. Efficacy and safety of rituximab for relapsing-remitting multiple sclerosis: A systematic review and meta-analysis. Autoimmunity Reviews. 2019;18:542–548.PubMedCrossRef Hu Y, Nie H, Yu H-H, et al. Efficacy and safety of rituximab for relapsing-remitting multiple sclerosis: A systematic review and meta-analysis. Autoimmunity Reviews. 2019;18:542–548.PubMedCrossRef
88.
Zurück zum Zitat van Vollenhoven RF, Fleischmann RM, Furst DE, et al. Longterm Safety of Rituximab: Final Report of the Rheumatoid Arthritis Global Clinical Trial Program over 11 Years. J Rheumatol. 2015;42:1761–1766.PubMedCrossRef van Vollenhoven RF, Fleischmann RM, Furst DE, et al. Longterm Safety of Rituximab: Final Report of the Rheumatoid Arthritis Global Clinical Trial Program over 11 Years. J Rheumatol. 2015;42:1761–1766.PubMedCrossRef
89.
Zurück zum Zitat Evens AM, Jovanovic BD, Su Y-C, et al. Rituximab-associated hepatitis B virus (HBV) reactivation in lymphoproliferative diseases: meta-analysis and examination of FDA safety reports. Ann Oncol. 2011;22:1170–1180.PubMedCrossRef Evens AM, Jovanovic BD, Su Y-C, et al. Rituximab-associated hepatitis B virus (HBV) reactivation in lymphoproliferative diseases: meta-analysis and examination of FDA safety reports. Ann Oncol. 2011;22:1170–1180.PubMedCrossRef
90.
Zurück zum Zitat Berger JR, Malik V, Lacey S, et al. Progressive multifocal leukoencephalopathy in rituximab-treated rheumatic diseases: a rare event. J Neurovirol. 2018;24:323–331.PubMedPubMedCentralCrossRef Berger JR, Malik V, Lacey S, et al. Progressive multifocal leukoencephalopathy in rituximab-treated rheumatic diseases: a rare event. J Neurovirol. 2018;24:323–331.PubMedPubMedCentralCrossRef
91.
Zurück zum Zitat Hauser SL, Bar-Or A, Comi G, et al. Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis. New England Journal of Medicine. 2017;376:221–234.CrossRef Hauser SL, Bar-Or A, Comi G, et al. Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis. New England Journal of Medicine. 2017;376:221–234.CrossRef
92.
Zurück zum Zitat Turner B, Cree BAC, Kappos L, et al. Ocrelizumab efficacy in subgroups of patients with relapsing multiple sclerosis. J Neurol. 2019;266:1182–1193.PubMedPubMedCentralCrossRef Turner B, Cree BAC, Kappos L, et al. Ocrelizumab efficacy in subgroups of patients with relapsing multiple sclerosis. J Neurol. 2019;266:1182–1193.PubMedPubMedCentralCrossRef
93.
Zurück zum Zitat Montalban X, Hauser SL, Kappos L, et al. Ocrelizumab versus Placebo in Primary Progressive Multiple Sclerosis. New England Journal of Medicine. 2017;376:209–220.CrossRef Montalban X, Hauser SL, Kappos L, et al. Ocrelizumab versus Placebo in Primary Progressive Multiple Sclerosis. New England Journal of Medicine. 2017;376:209–220.CrossRef
94.
Zurück zum Zitat Emery P, Rigby W, Tak PP, et al. Safety with Ocrelizumab in Rheumatoid Arthritis: Results from the Ocrelizumab Phase III Program. Schooling CM, editor. PLoS ONE. 2014;9:e87379. Emery P, Rigby W, Tak PP, et al. Safety with Ocrelizumab in Rheumatoid Arthritis: Results from the Ocrelizumab Phase III Program. Schooling CM, editor. PLoS ONE. 2014;9:e87379.
95.
Zurück zum Zitat Ciardi MR, Iannetta M, Zingaropoli MA, et al. Reactivation of Hepatitis B Virus With Immune-Escape Mutations After Ocrelizumab Treatment for Multiple Sclerosis. Open Forum Infect Dis. 2019;6:ofy356.PubMedCrossRef Ciardi MR, Iannetta M, Zingaropoli MA, et al. Reactivation of Hepatitis B Virus With Immune-Escape Mutations After Ocrelizumab Treatment for Multiple Sclerosis. Open Forum Infect Dis. 2019;6:ofy356.PubMedCrossRef
96.
Zurück zum Zitat ECTRIMS 2019 – Oral Presentations. Mult Scler. 2019;25:3–130. ECTRIMS 2019 – Oral Presentations. Mult Scler. 2019;25:3–130.
97.
Zurück zum Zitat Bar-Or A, Grove RA, Austin DJ, et al. Subcutaneous ofatumumab in patients with relapsing-remitting multiple sclerosis: The MIRROR study. Neurology. 2018;90:e1805–e1814.PubMedPubMedCentralCrossRef Bar-Or A, Grove RA, Austin DJ, et al. Subcutaneous ofatumumab in patients with relapsing-remitting multiple sclerosis: The MIRROR study. Neurology. 2018;90:e1805–e1814.PubMedPubMedCentralCrossRef
98.
Zurück zum Zitat Teeling JL, French RR, Cragg MS, et al. Characterization of new human CD20 monoclonal antibodies with potent cytolytic activity against non-Hodgkin lymphomas. Blood. 2004;104:1793–1800.PubMedCrossRef Teeling JL, French RR, Cragg MS, et al. Characterization of new human CD20 monoclonal antibodies with potent cytolytic activity against non-Hodgkin lymphomas. Blood. 2004;104:1793–1800.PubMedCrossRef
99.
Zurück zum Zitat Hauser SL, Bar-Or A, Cohen JA, et al. Ofatumumab versus Teriflunomide in Multiple Sclerosis. New England Journal of Medicine. 2020;383:546–557.CrossRef Hauser SL, Bar-Or A, Cohen JA, et al. Ofatumumab versus Teriflunomide in Multiple Sclerosis. New England Journal of Medicine. 2020;383:546–557.CrossRef
100.
Zurück zum Zitat Payandeh Z, Bahrami AA, Hoseinpoor R, et al. The applications of anti-CD20 antibodies to treat various B cells disorders. Biomedicine & Pharmacotherapy. 2019;109:2415–2426.CrossRef Payandeh Z, Bahrami AA, Hoseinpoor R, et al. The applications of anti-CD20 antibodies to treat various B cells disorders. Biomedicine & Pharmacotherapy. 2019;109:2415–2426.CrossRef
101.
Zurück zum Zitat Fox E, Lovett-Racke AE, Gormley M, et al. A phase 2 multicenter study of ublituximab, a novel glycoengineered anti-CD20 monoclonal antibody, in patients with relapsing forms of multiple sclerosis. Mult Scler. 2020;1352458520918375. Fox E, Lovett-Racke AE, Gormley M, et al. A phase 2 multicenter study of ublituximab, a novel glycoengineered anti-CD20 monoclonal antibody, in patients with relapsing forms of multiple sclerosis. Mult Scler. 2020;1352458520918375.
102.
Zurück zum Zitat Sondermann P, Huber R, Oosthuizen V, et al. The 3.2-A crystal structure of the human IgG1 Fc fragment-Fc gammaRIII complex. Nature. 2000;406:267–273.PubMedCrossRef Sondermann P, Huber R, Oosthuizen V, et al. The 3.2-A crystal structure of the human IgG1 Fc fragment-Fc gammaRIII complex. Nature. 2000;406:267–273.PubMedCrossRef
103.
Zurück zum Zitat Koene HR, Kleijer M, Algra J, et al. Fc gammaRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell Fc gammaRIIIa, independently of the Fc gammaRIIIa-48L/R/H phenotype. Blood. 1997;90:1109–1114.PubMedCrossRef Koene HR, Kleijer M, Algra J, et al. Fc gammaRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell Fc gammaRIIIa, independently of the Fc gammaRIIIa-48L/R/H phenotype. Blood. 1997;90:1109–1114.PubMedCrossRef
104.
Zurück zum Zitat Wu J, Edberg JC, Redecha PB, et al. A novel polymorphism of FcgammaRIIIa (CD16) alters receptor function and predisposes to autoimmune disease. J Clin Invest. 1997;100:1059–1070.PubMedPubMedCentralCrossRef Wu J, Edberg JC, Redecha PB, et al. A novel polymorphism of FcgammaRIIIa (CD16) alters receptor function and predisposes to autoimmune disease. J Clin Invest. 1997;100:1059–1070.PubMedPubMedCentralCrossRef
105.
Zurück zum Zitat Vance BA, Huizinga TW, Wardwell K, et al. Binding of monomeric human IgG defines an expression polymorphism of Fc gamma RIII on large granular lymphocyte/natural killer cells. J Immunol. 1993;151:6429–6439.PubMed Vance BA, Huizinga TW, Wardwell K, et al. Binding of monomeric human IgG defines an expression polymorphism of Fc gamma RIII on large granular lymphocyte/natural killer cells. J Immunol. 1993;151:6429–6439.PubMed
106.
Zurück zum Zitat Hatjiharissi E, Xu L, Santos DD, et al. Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism. Blood. 2007;110:2561–2564.PubMedPubMedCentralCrossRef Hatjiharissi E, Xu L, Santos DD, et al. Increased natural killer cell expression of CD16, augmented binding and ADCC activity to rituximab among individuals expressing the Fc{gamma}RIIIa-158 V/V and V/F polymorphism. Blood. 2007;110:2561–2564.PubMedPubMedCentralCrossRef
107.
Zurück zum Zitat Cartron G, Dacheux L, Salles G, et al. Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcγRIIIa gene. Blood. 2002;99:754–758.PubMedCrossRef Cartron G, Dacheux L, Salles G, et al. Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcγRIIIa gene. Blood. 2002;99:754–758.PubMedCrossRef
108.
Zurück zum Zitat Treon SP, Hansen M, Branagan AR, et al. Polymorphisms in FcγRIIIA (CD16) Receptor Expression Are Associated With Clinical Response to Rituximab in Waldenström’s Macroglobulinemia. JCO. 2005;23:474–481.CrossRef Treon SP, Hansen M, Branagan AR, et al. Polymorphisms in FcγRIIIA (CD16) Receptor Expression Are Associated With Clinical Response to Rituximab in Waldenström’s Macroglobulinemia. JCO. 2005;23:474–481.CrossRef
109.
Zurück zum Zitat Ruyssen-Witrand A, Rouanet S, Combe B, et al. Fcγ receptor type IIIA polymorphism influences treatment outcomes in patients with rheumatoid arthritis treated with rituximab. Ann Rheum Dis. 2012;71:875–877.PubMedCrossRef Ruyssen-Witrand A, Rouanet S, Combe B, et al. Fcγ receptor type IIIA polymorphism influences treatment outcomes in patients with rheumatoid arthritis treated with rituximab. Ann Rheum Dis. 2012;71:875–877.PubMedCrossRef
110.
Zurück zum Zitat Quartuccio L, Fabris M, Pontarini E, et al. The 158VV Fcgamma receptor 3A genotype is associated with response to rituximab in rheumatoid arthritis: results of an Italian multicentre study. Ann Rheum Dis. 2014;73:716–721.PubMedCrossRef Quartuccio L, Fabris M, Pontarini E, et al. The 158VV Fcgamma receptor 3A genotype is associated with response to rituximab in rheumatoid arthritis: results of an Italian multicentre study. Ann Rheum Dis. 2014;73:716–721.PubMedCrossRef
111.
Zurück zum Zitat Weng W-K, Levy R. Two immunoglobulin G fragment C receptor polymorphisms independently predict response to rituximab in patients with follicular lymphoma. J Clin Oncol. 2003;21:3940–3947.PubMedCrossRef Weng W-K, Levy R. Two immunoglobulin G fragment C receptor polymorphisms independently predict response to rituximab in patients with follicular lymphoma. J Clin Oncol. 2003;21:3940–3947.PubMedCrossRef
112.
Zurück zum Zitat Persky DO, Dornan D, Goldman BH, et al. Fc gamma receptor 3a genotype predicts overall survival in follicular lymphoma patients treated on SWOG trials with combined monoclonal antibody plus chemotherapy but not chemotherapy alone. Haematologica. 2012;97:937–942.PubMedPubMedCentralCrossRef Persky DO, Dornan D, Goldman BH, et al. Fc gamma receptor 3a genotype predicts overall survival in follicular lymphoma patients treated on SWOG trials with combined monoclonal antibody plus chemotherapy but not chemotherapy alone. Haematologica. 2012;97:937–942.PubMedPubMedCentralCrossRef
113.
Zurück zum Zitat Ahlgrimm M, Pfreundschuh M, Kreuz M, et al. The impact of Fc-γ receptor polymorphisms in elderly patients with diffuse large B-cell lymphoma treated with CHOP with or without rituximab. Blood. 2011;118:4657–4662.PubMedPubMedCentralCrossRef Ahlgrimm M, Pfreundschuh M, Kreuz M, et al. The impact of Fc-γ receptor polymorphisms in elderly patients with diffuse large B-cell lymphoma treated with CHOP with or without rituximab. Blood. 2011;118:4657–4662.PubMedPubMedCentralCrossRef
114.
Zurück zum Zitat Keller CW, Ruck T, McHugh D, et al. Impact of FcγR variants on the response to alemtuzumab in multiple sclerosis. Ann Clin Transl Neurol. 2019;6:2586–2594.PubMedPubMedCentralCrossRef Keller CW, Ruck T, McHugh D, et al. Impact of FcγR variants on the response to alemtuzumab in multiple sclerosis. Ann Clin Transl Neurol. 2019;6:2586–2594.PubMedPubMedCentralCrossRef
115.
Zurück zum Zitat Kim S-H, Jeong IH, Hyun J-W, et al. Treatment Outcomes With Rituximab in 100 Patients With Neuromyelitis Optica: Influence of FCGR3A Polymorphisms on the Therapeutic Response to Rituximab. JAMA Neurol. 2015;72:989–995.PubMedCrossRef Kim S-H, Jeong IH, Hyun J-W, et al. Treatment Outcomes With Rituximab in 100 Patients With Neuromyelitis Optica: Influence of FCGR3A Polymorphisms on the Therapeutic Response to Rituximab. JAMA Neurol. 2015;72:989–995.PubMedCrossRef
116.
Zurück zum Zitat Anolik JH, Campbell D, Felgar RE, et al. The relationship of FcgammaRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus. Arthritis Rheum. 2003;48:455–459.PubMedCrossRef Anolik JH, Campbell D, Felgar RE, et al. The relationship of FcgammaRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus. Arthritis Rheum. 2003;48:455–459.PubMedCrossRef
117.
Zurück zum Zitat Dall’Ozzo S, Tartas S, Paintaud G, et al. Rituximab-dependent cytotoxicity by natural killer cells: influence of FCGR3A polymorphism on the concentration-effect relationship. Cancer Res. 2004;64:4664–4669.PubMedCrossRef Dall’Ozzo S, Tartas S, Paintaud G, et al. Rituximab-dependent cytotoxicity by natural killer cells: influence of FCGR3A polymorphism on the concentration-effect relationship. Cancer Res. 2004;64:4664–4669.PubMedCrossRef
118.
Zurück zum Zitat Warmerdam PA, van de Winkel JG, Vlug A, et al. A single amino acid in the second Ig-like domain of the human Fc gamma receptor II is critical for human IgG2 binding. J Immunol. 1991;147:1338–1343.PubMed Warmerdam PA, van de Winkel JG, Vlug A, et al. A single amino acid in the second Ig-like domain of the human Fc gamma receptor II is critical for human IgG2 binding. J Immunol. 1991;147:1338–1343.PubMed
119.
Zurück zum Zitat Musolino A, Naldi N, Bortesi B, et al. Immunoglobulin G fragment C receptor polymorphisms and clinical efficacy of trastuzumab-based therapy in patients with HER-2/neu-positive metastatic breast cancer. J Clin Oncol. 2008;26:1789–1796.PubMedCrossRef Musolino A, Naldi N, Bortesi B, et al. Immunoglobulin G fragment C receptor polymorphisms and clinical efficacy of trastuzumab-based therapy in patients with HER-2/neu-positive metastatic breast cancer. J Clin Oncol. 2008;26:1789–1796.PubMedCrossRef
120.
Zurück zum Zitat Bibeau F, Lopez-Crapez E, Di Fiore F, et al. Impact of Fc{gamma}RIIa-Fc{gamma}RIIIa polymorphisms and KRAS mutations on the clinical outcome of patients with metastatic colorectal cancer treated with cetuximab plus irinotecan. J Clin Oncol. 2009;27:1122–1129.PubMedCrossRef Bibeau F, Lopez-Crapez E, Di Fiore F, et al. Impact of Fc{gamma}RIIa-Fc{gamma}RIIIa polymorphisms and KRAS mutations on the clinical outcome of patients with metastatic colorectal cancer treated with cetuximab plus irinotecan. J Clin Oncol. 2009;27:1122–1129.PubMedCrossRef
121.
Zurück zum Zitat Nishio M, Endo T, Fujimoto K, et al. FCGR3A-158V/F polymorphism may correlate with the levels of immunoglobulin in patients with non-Hodgkin’s lymphoma after rituximab treatment as an adjuvant to autologous stem cell transplantation. European Journal of Haematology. 2009;82:143–147.PubMedCrossRef Nishio M, Endo T, Fujimoto K, et al. FCGR3A-158V/F polymorphism may correlate with the levels of immunoglobulin in patients with non-Hodgkin’s lymphoma after rituximab treatment as an adjuvant to autologous stem cell transplantation. European Journal of Haematology. 2009;82:143–147.PubMedCrossRef
122.
Zurück zum Zitat Sakai H, Tanaka Y, Tazawa H, et al. Effect of Fc-γ Receptor Polymorphism on Rituximab-Mediated B Cell Depletion in ABO-Incompatible Adult Living Donor Liver Transplantation. Transplant Direct. 2017;3:e164.PubMedPubMedCentralCrossRef Sakai H, Tanaka Y, Tazawa H, et al. Effect of Fc-γ Receptor Polymorphism on Rituximab-Mediated B Cell Depletion in ABO-Incompatible Adult Living Donor Liver Transplantation. Transplant Direct. 2017;3:e164.PubMedPubMedCentralCrossRef
123.
Zurück zum Zitat Ajeganova S, Tesfa D, Hägglund H, et al. Effect of FCGR polymorphism on the occurrence of late-onset neutropenia and flare-free survival in rheumatic patients treated with rituximab. Arthritis Research & Therapy. 2017;19:44.CrossRef Ajeganova S, Tesfa D, Hägglund H, et al. Effect of FCGR polymorphism on the occurrence of late-onset neutropenia and flare-free survival in rheumatic patients treated with rituximab. Arthritis Research & Therapy. 2017;19:44.CrossRef
124.
Zurück zum Zitat Keane C, Nourse JP, Crooks P, et al. Homozygous FCGR3A-158V alleles predispose to late onset neutropenia after CHOP-R for diffuse large B-cell lymphoma: Impact of LON and FCGR3A-V158F in DLBCL. Internal Medicine Journal. 2012;42:1113–1119.PubMedCrossRef Keane C, Nourse JP, Crooks P, et al. Homozygous FCGR3A-158V alleles predispose to late onset neutropenia after CHOP-R for diffuse large B-cell lymphoma: Impact of LON and FCGR3A-V158F in DLBCL. Internal Medicine Journal. 2012;42:1113–1119.PubMedCrossRef
125.
Zurück zum Zitat Weng W-K, Negrin RS, Lavori P, et al. Immunoglobulin G Fc Receptor FcγRIIIa 158 V/F Polymorphism Correlates With Rituximab-Induced Neutropenia After Autologous Transplantation in Patients With Non-Hodgkin’s Lymphoma. Journal of Clinical Oncology. 2010;28:279–284.PubMedCrossRef Weng W-K, Negrin RS, Lavori P, et al. Immunoglobulin G Fc Receptor FcγRIIIa 158 V/F Polymorphism Correlates With Rituximab-Induced Neutropenia After Autologous Transplantation in Patients With Non-Hodgkin’s Lymphoma. Journal of Clinical Oncology. 2010;28:279–284.PubMedCrossRef
126.
Zurück zum Zitat Li S-C, Chen Y-C, Evens AM, et al. Rituximab-induced late onset neutropenia in newly-diagnosed B-cell lymphoma correlates with Fc receptor FcγRIIIa 158(V/F) polymorphism. American Journal of Hematology. 2010;85:810–812.PubMedCrossRef Li S-C, Chen Y-C, Evens AM, et al. Rituximab-induced late onset neutropenia in newly-diagnosed B-cell lymphoma correlates with Fc receptor FcγRIIIa 158(V/F) polymorphism. American Journal of Hematology. 2010;85:810–812.PubMedCrossRef
127.
Zurück zum Zitat Hincks I, Woodcock BE, Thachil J. Is Rituximab-induced Late-onset Neutropenia a good prognostic indicator in lymphoproliferatve disorders?: Correspondence. British Journal of Haematology. 2011;153:411–413.PubMedCrossRef Hincks I, Woodcock BE, Thachil J. Is Rituximab-induced Late-onset Neutropenia a good prognostic indicator in lymphoproliferatve disorders?: Correspondence. British Journal of Haematology. 2011;153:411–413.PubMedCrossRef
128.
Zurück zum Zitat Rigal J, Ciron J, Lépine Z, et al. Late-onset neutropenia after RITUXIMAB therapy for multiple sclerosis, neuromyelitis optica spectrum disorders and MOG-antibody-associated diseases. Mult Scler Relat Disord. 2020;41:102019.PubMedCrossRef Rigal J, Ciron J, Lépine Z, et al. Late-onset neutropenia after RITUXIMAB therapy for multiple sclerosis, neuromyelitis optica spectrum disorders and MOG-antibody-associated diseases. Mult Scler Relat Disord. 2020;41:102019.PubMedCrossRef
129.
Zurück zum Zitat Lee YH, Bae S-C. Associations between PTPRC rs10919563 A/G and FCGR2A R131H polymorphisms and responsiveness to TNF blockers in rheumatoid arthritis: a meta-analysis. Rheumatol Int. 2016;36:837–844.PubMedCrossRef Lee YH, Bae S-C. Associations between PTPRC rs10919563 A/G and FCGR2A R131H polymorphisms and responsiveness to TNF blockers in rheumatoid arthritis: a meta-analysis. Rheumatol Int. 2016;36:837–844.PubMedCrossRef
130.
Zurück zum Zitat Cañete JD, Suárez B, Hernández MV, et al. Influence of variants of Fc gamma receptors IIA and IIIA on the American College of Rheumatology and European League Against Rheumatism responses to anti-tumour necrosis factor alpha therapy in rheumatoid arthritis. Ann Rheum Dis. 2009;68:1547–1552.PubMedCrossRef Cañete JD, Suárez B, Hernández MV, et al. Influence of variants of Fc gamma receptors IIA and IIIA on the American College of Rheumatology and European League Against Rheumatism responses to anti-tumour necrosis factor alpha therapy in rheumatoid arthritis. Ann Rheum Dis. 2009;68:1547–1552.PubMedCrossRef
131.
Zurück zum Zitat Tutuncu Z, Kavanaugh A, Zvaifler N, et al. Fcγ receptor type IIIA polymorphisms influence treatment outcomes in patients with inflammatory arthritis treated with tumor necrosis factor α-blocking agents. Arthritis Rheum. 2005;52:2693–2696.PubMedCrossRef Tutuncu Z, Kavanaugh A, Zvaifler N, et al. Fcγ receptor type IIIA polymorphisms influence treatment outcomes in patients with inflammatory arthritis treated with tumor necrosis factor α-blocking agents. Arthritis Rheum. 2005;52:2693–2696.PubMedCrossRef
132.
Zurück zum Zitat Ternant D, Berkane Z, Picon L, et al. Assessment of the Influence of Inflammation and FCGR3A Genotype on Infliximab Pharmacokinetics and Time to Relapse in Patients with Crohn’s Disease. Clin Pharmacokinet. 2015;54:551–562.PubMedCrossRef Ternant D, Berkane Z, Picon L, et al. Assessment of the Influence of Inflammation and FCGR3A Genotype on Infliximab Pharmacokinetics and Time to Relapse in Patients with Crohn’s Disease. Clin Pharmacokinet. 2015;54:551–562.PubMedCrossRef
133.
Zurück zum Zitat Borvak J, Richardson J, Medesan C, et al. Functional expression of the MHC class I-related receptor, FcRn, in endothelial cells of mice. Int Immunol. 1998;10:1289–1298.PubMedCrossRef Borvak J, Richardson J, Medesan C, et al. Functional expression of the MHC class I-related receptor, FcRn, in endothelial cells of mice. Int Immunol. 1998;10:1289–1298.PubMedCrossRef
134.
Zurück zum Zitat Baldwin WM, Valujskikh A, Fairchild RL. The neonatal Fc receptor: Key to homeostasic control of IgG and IgG-related biopharmaceuticals. American Journal of Transplantation. 2019;19:1881–1887.PubMedPubMedCentral Baldwin WM, Valujskikh A, Fairchild RL. The neonatal Fc receptor: Key to homeostasic control of IgG and IgG-related biopharmaceuticals. American Journal of Transplantation. 2019;19:1881–1887.PubMedPubMedCentral
135.
Zurück zum Zitat Gouilleux-Gruart V, Chapel H, Chevret S, et al. Efficiency of immunoglobulin G replacement therapy in common variable immunodeficiency: correlations with clinical phenotype and polymorphism of the neonatal Fc receptor: IgG efficiency and FcRn in CVID. Clinical & Experimental Immunology. 2013;171:186–194.CrossRef Gouilleux-Gruart V, Chapel H, Chevret S, et al. Efficiency of immunoglobulin G replacement therapy in common variable immunodeficiency: correlations with clinical phenotype and polymorphism of the neonatal Fc receptor: IgG efficiency and FcRn in CVID. Clinical & Experimental Immunology. 2013;171:186–194.CrossRef
136.
Zurück zum Zitat Billiet T, Dreesen E, Cleynen I, et al. A Genetic Variation in the Neonatal Fc-Receptor Affects Anti-TNF Drug Concentrations in Inflammatory Bowel Disease: American Journal of Gastroenterology. 2016;111:1438–1445.CrossRef Billiet T, Dreesen E, Cleynen I, et al. A Genetic Variation in the Neonatal Fc-Receptor Affects Anti-TNF Drug Concentrations in Inflammatory Bowel Disease: American Journal of Gastroenterology. 2016;111:1438–1445.CrossRef
137.
Zurück zum Zitat Passot C, Azzopardi N, Renault S, et al. Influence of FCGRT gene polymorphisms on pharmacokinetics of therapeutic antibodies. mAbs. 2013;5:614–619.PubMedPubMedCentralCrossRef Passot C, Azzopardi N, Renault S, et al. Influence of FCGRT gene polymorphisms on pharmacokinetics of therapeutic antibodies. mAbs. 2013;5:614–619.PubMedPubMedCentralCrossRef
138.
Zurück zum Zitat Ruyssen-Witrand A, Rouanet S, Combe B, et al. Association between -871C>T promoter polymorphism in the B-cell activating factor gene and the response to rituximab in rheumatoid arthritis patients. Rheumatology. 2013;52:636–641.PubMedCrossRef Ruyssen-Witrand A, Rouanet S, Combe B, et al. Association between -871C>T promoter polymorphism in the B-cell activating factor gene and the response to rituximab in rheumatoid arthritis patients. Rheumatology. 2013;52:636–641.PubMedCrossRef
139.
Zurück zum Zitat Alberici F, Smith RM, Fonseca M, et al. Association of a TNFSF13B (BAFF) regulatory region single nucleotide polymorphism with response to rituximab in antineutrophil cytoplasmic antibody–associated vasculitis. Journal of Allergy and Clinical Immunology. 2017;139:1684-1687.e10.CrossRef Alberici F, Smith RM, Fonseca M, et al. Association of a TNFSF13B (BAFF) regulatory region single nucleotide polymorphism with response to rituximab in antineutrophil cytoplasmic antibody–associated vasculitis. Journal of Allergy and Clinical Immunology. 2017;139:1684-1687.e10.CrossRef
140.
Zurück zum Zitat Fabris M, Quartuccio L, Vital E, et al. The TTTT B lymphocyte stimulator promoter haplotype is associated with good response to rituximab therapy in seropositive rheumatoid arthritis resistant to tumor necrosis factor blockers. Arthritis & Rheumatism. 2013;65:88–97.CrossRef Fabris M, Quartuccio L, Vital E, et al. The TTTT B lymphocyte stimulator promoter haplotype is associated with good response to rituximab therapy in seropositive rheumatoid arthritis resistant to tumor necrosis factor blockers. Arthritis & Rheumatism. 2013;65:88–97.CrossRef
141.
Zurück zum Zitat Steri M, Orrù V, Idda ML, et al. Overexpression of the Cytokine BAFF and Autoimmunity Risk. New England Journal of Medicine. 2017;376:1615–1626.CrossRef Steri M, Orrù V, Idda ML, et al. Overexpression of the Cytokine BAFF and Autoimmunity Risk. New England Journal of Medicine. 2017;376:1615–1626.CrossRef
142.
Zurück zum Zitat Comabella M. Neuroimmunology: B cells and variant BAFF in autoimmune disease. Nat Rev Neurol. 2017;13:453–454.PubMedCrossRef Comabella M. Neuroimmunology: B cells and variant BAFF in autoimmune disease. Nat Rev Neurol. 2017;13:453–454.PubMedCrossRef
143.
Zurück zum Zitat Jin X, Ding H, Ding N, et al. Homozygous A polymorphism of the complement C1qA276 correlates with prolonged overall survival in patients with diffuse large B cell lymphoma treated with R-CHOP. J Hematol Oncol. 2012;5:51.PubMedPubMedCentralCrossRef Jin X, Ding H, Ding N, et al. Homozygous A polymorphism of the complement C1qA276 correlates with prolonged overall survival in patients with diffuse large B cell lymphoma treated with R-CHOP. J Hematol Oncol. 2012;5:51.PubMedPubMedCentralCrossRef
144.
Zurück zum Zitat Stegert M, Bock M, Trendelenburg M. Clinical presentation of human C1q deficiency: How much of a lupus? Mol Immunol. 2015;67:3–11.PubMedCrossRef Stegert M, Bock M, Trendelenburg M. Clinical presentation of human C1q deficiency: How much of a lupus? Mol Immunol. 2015;67:3–11.PubMedCrossRef
145.
Zurück zum Zitat Racila DM, Sontheimer CJ, Sheffield A, et al. Homozygous single nucleotide polymorphism of the complement C1QA gene is associated with decreased levels of C1q in patients with subacute cutaneous lupus erythematosus. Lupus. 2003;12:124–132.PubMedCrossRef Racila DM, Sontheimer CJ, Sheffield A, et al. Homozygous single nucleotide polymorphism of the complement C1QA gene is associated with decreased levels of C1q in patients with subacute cutaneous lupus erythematosus. Lupus. 2003;12:124–132.PubMedCrossRef
146.
Zurück zum Zitat Racila E, Link BK, Weng W-K, et al. A Polymorphism in the Complement Component C1qA Correlates with Prolonged Response Following Rituximab Therapy of Follicular Lymphoma. Clinical Cancer Research. 2008;14:6697–6703.PubMedPubMedCentralCrossRef Racila E, Link BK, Weng W-K, et al. A Polymorphism in the Complement Component C1qA Correlates with Prolonged Response Following Rituximab Therapy of Follicular Lymphoma. Clinical Cancer Research. 2008;14:6697–6703.PubMedPubMedCentralCrossRef
147.
Zurück zum Zitat Ding H, Jin X, Ding N, et al. Single nucleotide polymorphisms of CD20 gene and their relationship with clinical efficacy of R-CHOP in patients with diffuse large B cell lymphoma. Cancer Cell Int. 2013;13:58.PubMedPubMedCentralCrossRef Ding H, Jin X, Ding N, et al. Single nucleotide polymorphisms of CD20 gene and their relationship with clinical efficacy of R-CHOP in patients with diffuse large B cell lymphoma. Cancer Cell Int. 2013;13:58.PubMedPubMedCentralCrossRef
148.
Zurück zum Zitat Terui Y, Mishima Y, Sugimura N, et al. Identification of CD20 C-terminal deletion mutations associated with loss of CD20 expression in non-Hodgkin’s lymphoma. Clin Cancer Res. 2009;15:2523–2530.PubMedCrossRef Terui Y, Mishima Y, Sugimura N, et al. Identification of CD20 C-terminal deletion mutations associated with loss of CD20 expression in non-Hodgkin’s lymphoma. Clin Cancer Res. 2009;15:2523–2530.PubMedCrossRef
149.
Zurück zum Zitat Fabris M, Quartuccio L, Lombardi S, et al. The CC homozygosis of the -174G>C IL-6 polymorphism predicts a lower efficacy of rituximab therapy in rheumatoid arthritis. Autoimmun Rev. 2012;11:315–320.PubMedCrossRef Fabris M, Quartuccio L, Lombardi S, et al. The CC homozygosis of the -174G>C IL-6 polymorphism predicts a lower efficacy of rituximab therapy in rheumatoid arthritis. Autoimmun Rev. 2012;11:315–320.PubMedCrossRef
150.
Zurück zum Zitat Das S, Vital EM, Horton S, et al. Abatacept or tocilizumab after rituximab in rheumatoid arthritis? An exploratory study suggests non-response to rituximab is associated with persistently high IL-6 and better clinical response to IL-6 blocking therapy. Ann Rheum Dis. 2014;73:909–912.PubMedCrossRef Das S, Vital EM, Horton S, et al. Abatacept or tocilizumab after rituximab in rheumatoid arthritis? An exploratory study suggests non-response to rituximab is associated with persistently high IL-6 and better clinical response to IL-6 blocking therapy. Ann Rheum Dis. 2014;73:909–912.PubMedCrossRef
151.
Zurück zum Zitat Hu S, Chen Y, Sun X-D, et al. Association between IL-6-174G/C polymorphism and risk of multiple sclerosis: a meta-analysis. Genet Test Mol Biomarkers. 2014;18:127–130.PubMedCrossRef Hu S, Chen Y, Sun X-D, et al. Association between IL-6-174G/C polymorphism and risk of multiple sclerosis: a meta-analysis. Genet Test Mol Biomarkers. 2014;18:127–130.PubMedCrossRef
152.
Zurück zum Zitat Fonseca JE, Santos MJ, Canhão H, et al. Interleukin-6 as a key player in systemic inflammation and joint destruction. Autoimmun Rev. 2009;8:538–542.PubMedCrossRef Fonseca JE, Santos MJ, Canhão H, et al. Interleukin-6 as a key player in systemic inflammation and joint destruction. Autoimmun Rev. 2009;8:538–542.PubMedCrossRef
153.
Zurück zum Zitat Cohen SB, Emery P, Greenwald MW, et al. Rituximab for rheumatoid arthritis refractory to anti-tumor necrosis factor therapy: Results of a multicenter, randomized, double-blind, placebo-controlled, phase III trial evaluating primary efficacy and safety at twenty-four weeks. Arthritis Rheum. 2006;54:2793–2806.PubMedCrossRef Cohen SB, Emery P, Greenwald MW, et al. Rituximab for rheumatoid arthritis refractory to anti-tumor necrosis factor therapy: Results of a multicenter, randomized, double-blind, placebo-controlled, phase III trial evaluating primary efficacy and safety at twenty-four weeks. Arthritis Rheum. 2006;54:2793–2806.PubMedCrossRef
154.
Zurück zum Zitat Emery P, Fleischmann R, Filipowicz-Sosnowska A, et al. The efficacy and safety of rituximab in patients with active rheumatoid arthritis despite methotrexate treatment: results of a phase IIB randomized, double-blind, placebo-controlled, dose-ranging trial. Arthritis Rheum. 2006;54:1390–1400.PubMedCrossRef Emery P, Fleischmann R, Filipowicz-Sosnowska A, et al. The efficacy and safety of rituximab in patients with active rheumatoid arthritis despite methotrexate treatment: results of a phase IIB randomized, double-blind, placebo-controlled, dose-ranging trial. Arthritis Rheum. 2006;54:1390–1400.PubMedCrossRef
155.
156.
Zurück zum Zitat Salles G, Barrett M, Foà R, et al. Rituximab in B-Cell Hematologic Malignancies: A Review of 20 Years of Clinical Experience. Adv Ther. 2017;34:2232–2273.PubMedPubMedCentralCrossRef Salles G, Barrett M, Foà R, et al. Rituximab in B-Cell Hematologic Malignancies: A Review of 20 Years of Clinical Experience. Adv Ther. 2017;34:2232–2273.PubMedPubMedCentralCrossRef
157.
Zurück zum Zitat Coiffier B, Haioun C, Ketterer N, et al. Rituximab (anti-CD20 monoclonal antibody) for the treatment of patients with relapsing or refractory aggressive lymphoma: a multicenter phase II study. Blood. 1998;92:1927–1932.PubMed Coiffier B, Haioun C, Ketterer N, et al. Rituximab (anti-CD20 monoclonal antibody) for the treatment of patients with relapsing or refractory aggressive lymphoma: a multicenter phase II study. Blood. 1998;92:1927–1932.PubMed
158.
Zurück zum Zitat Kappos L, Li D, Calabresi PA, et al. Ocrelizumab in relapsing-remitting multiple sclerosis: a phase 2, randomised, placebo-controlled, multicentre trial. Lancet. 2011;378:1779–1787.PubMedCrossRef Kappos L, Li D, Calabresi PA, et al. Ocrelizumab in relapsing-remitting multiple sclerosis: a phase 2, randomised, placebo-controlled, multicentre trial. Lancet. 2011;378:1779–1787.PubMedCrossRef
159.
Zurück zum Zitat Morschhauser F, Marlton P, Vitolo U, et al. Results of a phase I/II study of ocrelizumab, a fully humanized anti-CD20 mAb, in patients with relapsed/refractory follicular lymphoma. Ann Oncol. 2010;21:1870–1876.PubMedCrossRef Morschhauser F, Marlton P, Vitolo U, et al. Results of a phase I/II study of ocrelizumab, a fully humanized anti-CD20 mAb, in patients with relapsed/refractory follicular lymphoma. Ann Oncol. 2010;21:1870–1876.PubMedCrossRef
160.
Zurück zum Zitat Rigby W, Tony H-P, Oelke K, et al. Safety and efficacy of ocrelizumab in patients with rheumatoid arthritis and an inadequate response to methotrexate: Results of a forty-eight-week randomized, double-blind, placebo-controlled, parallel-group phase III trial. Arthritis & Rheumatism. 2012;64:350–359.CrossRef Rigby W, Tony H-P, Oelke K, et al. Safety and efficacy of ocrelizumab in patients with rheumatoid arthritis and an inadequate response to methotrexate: Results of a forty-eight-week randomized, double-blind, placebo-controlled, parallel-group phase III trial. Arthritis & Rheumatism. 2012;64:350–359.CrossRef
161.
Zurück zum Zitat Tak PP, Mease PJ, Genovese MC, et al. Safety and efficacy of ocrelizumab in patients with rheumatoid arthritis and an inadequate response to at least one tumor necrosis factor inhibitor: Results of a forty-eight-week randomized, double-blind, placebo-controlled, parallel-group phase III trial. Arthritis & Rheumatism. 2012;64:360–370.CrossRef Tak PP, Mease PJ, Genovese MC, et al. Safety and efficacy of ocrelizumab in patients with rheumatoid arthritis and an inadequate response to at least one tumor necrosis factor inhibitor: Results of a forty-eight-week randomized, double-blind, placebo-controlled, parallel-group phase III trial. Arthritis & Rheumatism. 2012;64:360–370.CrossRef
162.
Zurück zum Zitat Coiffier B, Lepretre S, Pedersen LM, et al. Safety and efficacy of ofatumumab, a fully human monoclonal anti-CD20 antibody, in patients with relapsed or refractory B-cell chronic lymphocytic leukemia: a phase 1-2 study. Blood. 2008;111:1094–1100.PubMedCrossRef Coiffier B, Lepretre S, Pedersen LM, et al. Safety and efficacy of ofatumumab, a fully human monoclonal anti-CD20 antibody, in patients with relapsed or refractory B-cell chronic lymphocytic leukemia: a phase 1-2 study. Blood. 2008;111:1094–1100.PubMedCrossRef
163.
Zurück zum Zitat Freeman CL, Sehn LH. A tale of two antibodies: obinutuzumab versus rituximab. Br J Haematol. 2018;182:29–45.PubMedCrossRef Freeman CL, Sehn LH. A tale of two antibodies: obinutuzumab versus rituximab. Br J Haematol. 2018;182:29–45.PubMedCrossRef
164.
Zurück zum Zitat Mössner E, Brünker P, Moser S, et al. Increasing the efficacy of CD20 antibody therapy through the engineering of a new type II anti-CD20 antibody with enhanced direct and immune effector cell-mediated B-cell cytotoxicity. Blood. 2010;115:4393–4402.PubMedPubMedCentralCrossRef Mössner E, Brünker P, Moser S, et al. Increasing the efficacy of CD20 antibody therapy through the engineering of a new type II anti-CD20 antibody with enhanced direct and immune effector cell-mediated B-cell cytotoxicity. Blood. 2010;115:4393–4402.PubMedPubMedCentralCrossRef
165.
Zurück zum Zitat Goede V, Fischer K, Busch R, et al. Obinutuzumab plus chlorambucil in patients with CLL and coexisting conditions. N Engl J Med. 2014;370:1101–1110.PubMedCrossRef Goede V, Fischer K, Busch R, et al. Obinutuzumab plus chlorambucil in patients with CLL and coexisting conditions. N Engl J Med. 2014;370:1101–1110.PubMedCrossRef
166.
Zurück zum Zitat Marcus R, Davies A, Ando K, et al. Obinutuzumab for the First-Line Treatment of Follicular Lymphoma. N Engl J Med. 2017;377:1331–1344.PubMedCrossRef Marcus R, Davies A, Ando K, et al. Obinutuzumab for the First-Line Treatment of Follicular Lymphoma. N Engl J Med. 2017;377:1331–1344.PubMedCrossRef
167.
Zurück zum Zitat Le Garff-Tavernier M, Herbi L, de Romeuf C, et al. Antibody-dependent cellular cytotoxicity of the optimized anti-CD20 monoclonal antibody ublituximab on chronic lymphocytic leukemia cells with the 17p deletion. Leukemia. 2014;28:230–233.PubMedCrossRef Le Garff-Tavernier M, Herbi L, de Romeuf C, et al. Antibody-dependent cellular cytotoxicity of the optimized anti-CD20 monoclonal antibody ublituximab on chronic lymphocytic leukemia cells with the 17p deletion. Leukemia. 2014;28:230–233.PubMedCrossRef
168.
Zurück zum Zitat Babiker HM, Glode AE, Cooke LS, et al. Ublituximab for the treatment of CD20 positive B-cell malignancies. Expert Opinion on Investigational Drugs. 2018;27:407–412.PubMedCrossRef Babiker HM, Glode AE, Cooke LS, et al. Ublituximab for the treatment of CD20 positive B-cell malignancies. Expert Opinion on Investigational Drugs. 2018;27:407–412.PubMedCrossRef
169.
Zurück zum Zitat Kim DH, Jung HD, Kim JG, et al. FCGR3A gene polymorphisms may correlate with response to frontline R-CHOP therapy for diffuse large B-cell lymphoma. Blood. 2006;108:2720–2725.PubMedCrossRef Kim DH, Jung HD, Kim JG, et al. FCGR3A gene polymorphisms may correlate with response to frontline R-CHOP therapy for diffuse large B-cell lymphoma. Blood. 2006;108:2720–2725.PubMedCrossRef
170.
Zurück zum Zitat Kastbom A, Cöster L, Ärlestig L, et al. Influence of FCGR3A genotype on the therapeutic response to rituximab in rheumatoid arthritis: an observational cohort study. BMJ Open. 2012;2:e001524.PubMedPubMedCentralCrossRef Kastbom A, Cöster L, Ärlestig L, et al. Influence of FCGR3A genotype on the therapeutic response to rituximab in rheumatoid arthritis: an observational cohort study. BMJ Open. 2012;2:e001524.PubMedPubMedCentralCrossRef
171.
Zurück zum Zitat Pál I, Szamosi S, Hodosi K, et al. Effect of Fcγ-receptor 3a (FCGR3A) gene polymorphisms on rituximab therapy in Hungarian patients with rheumatoid arthritis. RMD Open. 2017;3:e000485.PubMedPubMedCentralCrossRef Pál I, Szamosi S, Hodosi K, et al. Effect of Fcγ-receptor 3a (FCGR3A) gene polymorphisms on rituximab therapy in Hungarian patients with rheumatoid arthritis. RMD Open. 2017;3:e000485.PubMedPubMedCentralCrossRef
Metadaten
Titel
The Pharmacogenetics of Rituximab: Potential Implications for Anti-CD20 Therapies in Multiple Sclerosis
verfasst von
Michael Zhong
Anneke van der Walt
Maria Pia Campagna
Jim Stankovich
Helmut Butzkueven
Vilija Jokubaitis
Publikationsdatum
01.10.2020
Verlag
Springer International Publishing
Erschienen in
Neurotherapeutics / Ausgabe 4/2020
Print ISSN: 1933-7213
Elektronische ISSN: 1878-7479
DOI
https://doi.org/10.1007/s13311-020-00950-2

Weitere Artikel der Ausgabe 4/2020

Neurotherapeutics 4/2020 Zur Ausgabe

Leitlinien kompakt für die Neurologie

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Demenzkranke durch Antipsychotika vielfach gefährdet

Demenz Nachrichten

Der Einsatz von Antipsychotika gegen psychische und Verhaltenssymptome in Zusammenhang mit Demenzerkrankungen erfordert eine sorgfältige Nutzen-Risiken-Abwägung. Neuen Erkenntnissen zufolge sind auf der Risikoseite weitere schwerwiegende Ereignisse zu berücksichtigen.

Nicht Creutzfeldt Jakob, sondern Abführtee-Vergiftung

29.05.2024 Hyponatriämie Nachrichten

Eine ältere Frau trinkt regelmäßig Sennesblättertee gegen ihre Verstopfung. Der scheint plötzlich gut zu wirken. Auf Durchfall und Erbrechen folgt allerdings eine Hyponatriämie. Nach deren Korrektur kommt es plötzlich zu progredienten Kognitions- und Verhaltensstörungen.

Schutz der Synapsen bei Alzheimer

29.05.2024 Morbus Alzheimer Nachrichten

Mit einem Neurotrophin-Rezeptor-Modulator lässt sich möglicherweise eine bestehende Alzheimerdemenz etwas abschwächen: Erste Phase-2-Daten deuten auf einen verbesserten Synapsenschutz.

Sozialer Aufstieg verringert Demenzgefahr

24.05.2024 Demenz Nachrichten

Ein hohes soziales Niveau ist mit die beste Versicherung gegen eine Demenz. Noch geringer ist das Demenzrisiko für Menschen, die sozial aufsteigen: Sie gewinnen fast zwei demenzfreie Lebensjahre. Umgekehrt steigt die Demenzgefahr beim sozialen Abstieg.

Update Neurologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.