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Erschienen in: Neurotherapeutics 1/2016

01.01.2016 | Review

Anti-B-Cell Therapies in Autoimmune Neurological Diseases: Rationale and Efficacy Trials

verfasst von: Harry Alexopoulos, Angie Biba, Marinos C. Dalakas

Erschienen in: Neurotherapeutics | Ausgabe 1/2016

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Abstract

B cells have an ever-increasing role in the etiopathology of a number of autoimmune neurological disorders, acting as antibody-producing cells and, most importantly, as sensors, coordinators, and regulators of the immune response. B cells, among other functions, regulate the T-cell activation process through their participation in antigen presentation and production of cytokines. The availability of monoclonal antibodies or fusion proteins against B-cell surface molecules or B-cell trophic factors bestows a rational approach for treating autoimmune neurological disorders, even when T cells are the main effector cells. This review summarizes basic aspects of B-cell biology, discusses the role(s) of B cells in neurological autoimmunity, and presents anti-B-cell drugs that are either currently on the market or are expected to be available in the near future for treating neurological autoimmune disorders.
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Literatur
1.
Zurück zum Zitat Eibel H, Kraus H, Sic H, Kienzler AK, Rizzi M. B cell biology: an overview. Curr Allergy Asthma Rep 2014;14:434.PubMedCrossRef Eibel H, Kraus H, Sic H, Kienzler AK, Rizzi M. B cell biology: an overview. Curr Allergy Asthma Rep 2014;14:434.PubMedCrossRef
2.
Zurück zum Zitat Pieper K, Grimbacher B, Eibel H. B-cell biology and development. J Allergy Clin Immunol 2013;131:959-971.PubMedCrossRef Pieper K, Grimbacher B, Eibel H. B-cell biology and development. J Allergy Clin Immunol 2013;131:959-971.PubMedCrossRef
3.
Zurück zum Zitat Weinstein E, Peeva E, Putterman C, Diamond B. B-cell biology. Rheum Dis Clin North Am 2004;30:159-174.PubMedCrossRef Weinstein E, Peeva E, Putterman C, Diamond B. B-cell biology. Rheum Dis Clin North Am 2004;30:159-174.PubMedCrossRef
4.
Zurück zum Zitat Kitano M, Moriyama S, Ando Y, et al. Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity. Immunity 2011;34:961-972.PubMedCrossRef Kitano M, Moriyama S, Ando Y, et al. Bcl6 protein expression shapes pre-germinal center B cell dynamics and follicular helper T cell heterogeneity. Immunity 2011;34:961-972.PubMedCrossRef
5.
Zurück zum Zitat O’Connor BP, Vogel LA, Zhang W, et al. Imprinting the fate of antigen-reactive B cells through the affinity of the B cell receptor. J Immunol 2006;177:7723-7732.PubMedPubMedCentralCrossRef O’Connor BP, Vogel LA, Zhang W, et al. Imprinting the fate of antigen-reactive B cells through the affinity of the B cell receptor. J Immunol 2006;177:7723-7732.PubMedPubMedCentralCrossRef
7.
Zurück zum Zitat Nutt SL, Hodgkin PD, Tarlinton DM, Corcoran LM. The generation of antibody-secreting plasma cells. Nat Rev Immunol 2015;15:160-171.PubMedCrossRef Nutt SL, Hodgkin PD, Tarlinton DM, Corcoran LM. The generation of antibody-secreting plasma cells. Nat Rev Immunol 2015;15:160-171.PubMedCrossRef
8.
Zurück zum Zitat Anolik JH, Barnard J, Owen T, et al. Delayed memory B cell recovery in peripheral blood and lymphoid tissue in systemic lupus erythematosus after B cell depletion therapy. Arthritis Rheum 2007;56:3044-3056.PubMedCrossRef Anolik JH, Barnard J, Owen T, et al. Delayed memory B cell recovery in peripheral blood and lymphoid tissue in systemic lupus erythematosus after B cell depletion therapy. Arthritis Rheum 2007;56:3044-3056.PubMedCrossRef
9.
Zurück zum Zitat Dass S, Rawstron AC, Vital EM, Henshaw K, McGonagle D, Emery P. Highly sensitive B cell analysis predicts response to rituximab therapy in rheumatoid arthritis. Arthritis Rheum 2008;58:2993-2999.PubMedCrossRef Dass S, Rawstron AC, Vital EM, Henshaw K, McGonagle D, Emery P. Highly sensitive B cell analysis predicts response to rituximab therapy in rheumatoid arthritis. Arthritis Rheum 2008;58:2993-2999.PubMedCrossRef
10.
Zurück zum Zitat Palanichamy A, Barnard J, Zheng B, et al. Novel human transitional B cell populations revealed by B cell depletion therapy. J Immunol 2009;182:5982-5993.PubMedPubMedCentralCrossRef Palanichamy A, Barnard J, Zheng B, et al. Novel human transitional B cell populations revealed by B cell depletion therapy. J Immunol 2009;182:5982-5993.PubMedPubMedCentralCrossRef
11.
Zurück zum Zitat Roll P, Dorner T, Tony HP. Anti-CD20 therapy in patients with rheumatoid arthritis: predictors of response and B cell subset regeneration after repeated treatment. Arthritis Rheum 2008;58:1566-1575.PubMedCrossRef Roll P, Dorner T, Tony HP. Anti-CD20 therapy in patients with rheumatoid arthritis: predictors of response and B cell subset regeneration after repeated treatment. Arthritis Rheum 2008;58:1566-1575.PubMedCrossRef
12.
Zurück zum Zitat Adlowitz DG, Barnard J, Biear JN, et al. Expansion of activated peripheral blood memory B cells in rheumatoid arthritis, impact of B cell depletion therapy, and biomarkers of response. PLoS One 2015;10:e0128269.PubMedPubMedCentralCrossRef Adlowitz DG, Barnard J, Biear JN, et al. Expansion of activated peripheral blood memory B cells in rheumatoid arthritis, impact of B cell depletion therapy, and biomarkers of response. PLoS One 2015;10:e0128269.PubMedPubMedCentralCrossRef
13.
Zurück zum Zitat Moore PA, Belvedere O, Orr A, et al. BLyS: member of the tumor necrosis factor family and B lymphocyte stimulator. Science 1999;285:260-263.PubMedCrossRef Moore PA, Belvedere O, Orr A, et al. BLyS: member of the tumor necrosis factor family and B lymphocyte stimulator. Science 1999;285:260-263.PubMedCrossRef
14.
Zurück zum Zitat Schneider P, MacKay F, Steiner V, et al. BAFF, a novel ligand of the tumor necrosis factor family, stimulates B cell growth. J Exp Med 1999;189:1747-1756.PubMedPubMedCentralCrossRef Schneider P, MacKay F, Steiner V, et al. BAFF, a novel ligand of the tumor necrosis factor family, stimulates B cell growth. J Exp Med 1999;189:1747-1756.PubMedPubMedCentralCrossRef
15.
Zurück zum Zitat Hahne M, Kataoka T, Schroter M, et al. APRIL, a new ligand of the tumor necrosis factor family, stimulates tumor cell growth. J Exp Med 1998;188:1185-1190.PubMedPubMedCentralCrossRef Hahne M, Kataoka T, Schroter M, et al. APRIL, a new ligand of the tumor necrosis factor family, stimulates tumor cell growth. J Exp Med 1998;188:1185-1190.PubMedPubMedCentralCrossRef
16.
Zurück zum Zitat Cachero TG, Schwartz IM, Qian F, et al. Formation of virus-like clusters is an intrinsic property of the tumor necrosis factor family member BAFF (B cell activating factor). Biochemistry 2006;45:2006-2013.PubMedCrossRef Cachero TG, Schwartz IM, Qian F, et al. Formation of virus-like clusters is an intrinsic property of the tumor necrosis factor family member BAFF (B cell activating factor). Biochemistry 2006;45:2006-2013.PubMedCrossRef
17.
Zurück zum Zitat Liu Y, Xu L, Opalka N, Kappler J, Shu HB, Zhang G. Crystal structure of sTALL-1 reveals a virus-like assembly of TNF family ligands. Cell 2002;108:383-394.PubMedCrossRef Liu Y, Xu L, Opalka N, Kappler J, Shu HB, Zhang G. Crystal structure of sTALL-1 reveals a virus-like assembly of TNF family ligands. Cell 2002;108:383-394.PubMedCrossRef
18.
Zurück zum Zitat Lopez-Fraga M, Fernandez R, Albar JP, Hahne M. Biologically active APRIL is secreted following intracellular processing in the Golgi apparatus by furin convertase. EMBO Rep 2001;2:945-951.PubMedPubMedCentralCrossRef Lopez-Fraga M, Fernandez R, Albar JP, Hahne M. Biologically active APRIL is secreted following intracellular processing in the Golgi apparatus by furin convertase. EMBO Rep 2001;2:945-951.PubMedPubMedCentralCrossRef
19.
Zurück zum Zitat Lavie F, Miceli-Richard C, Ittah M, Sellam J, Gottenberg JE, Mariette X. B-cell activating factor of the tumour necrosis factor family expression in blood monocytes and T cells from patients with primary Sjogren’s syndrome. Scand J Immunol 2008;67:185-192.PubMedCrossRef Lavie F, Miceli-Richard C, Ittah M, Sellam J, Gottenberg JE, Mariette X. B-cell activating factor of the tumour necrosis factor family expression in blood monocytes and T cells from patients with primary Sjogren’s syndrome. Scand J Immunol 2008;67:185-192.PubMedCrossRef
20.
Zurück zum Zitat Moreaux J, Legouffe E, Jourdan E, et al. BAFF and APRIL protect myeloma cells from apoptosis induced by interleukin 6 deprivation and dexamethasone. Blood 2004;103:3148-3157.PubMedCrossRef Moreaux J, Legouffe E, Jourdan E, et al. BAFF and APRIL protect myeloma cells from apoptosis induced by interleukin 6 deprivation and dexamethasone. Blood 2004;103:3148-3157.PubMedCrossRef
21.
Zurück zum Zitat Suzuki K, Setoyama Y, Yoshimoto K, Tsuzaka K, Abe T, Takeuchi T. Effect of interleukin-2 on synthesis of B cell activating factor belonging to the tumor necrosis factor family (BAFF) in human peripheral blood mononuclear cells. Cytokine 2008;44:44-48.PubMedCrossRef Suzuki K, Setoyama Y, Yoshimoto K, Tsuzaka K, Abe T, Takeuchi T. Effect of interleukin-2 on synthesis of B cell activating factor belonging to the tumor necrosis factor family (BAFF) in human peripheral blood mononuclear cells. Cytokine 2008;44:44-48.PubMedCrossRef
22.
Zurück zum Zitat Bossen C, Cachero TG, Tardivel A, et al. TACI, unlike BAFF-R, is solely activated by oligomeric BAFF and APRIL to support survival of activated B cells and plasmablasts. Blood 2008;111:1004-1012.PubMedCrossRef Bossen C, Cachero TG, Tardivel A, et al. TACI, unlike BAFF-R, is solely activated by oligomeric BAFF and APRIL to support survival of activated B cells and plasmablasts. Blood 2008;111:1004-1012.PubMedCrossRef
23.
Zurück zum Zitat Day ES, Cachero TG, Qian F, et al. Selectivity of BAFF/BLyS and APRIL for binding to the TNF family receptors BAFFR/BR3 and BCMA. Biochemistry 2005;44:1919-1931.PubMedCrossRef Day ES, Cachero TG, Qian F, et al. Selectivity of BAFF/BLyS and APRIL for binding to the TNF family receptors BAFFR/BR3 and BCMA. Biochemistry 2005;44:1919-1931.PubMedCrossRef
24.
Zurück zum Zitat Zhang L, Zheng S, Wu H, et al. Identification of BLyS (B lymphocyte stimulator), a non-myelin-associated protein, as a functional ligand for Nogo-66 receptor. J Neurosci 2009;29:6348-6352.PubMedCrossRef Zhang L, Zheng S, Wu H, et al. Identification of BLyS (B lymphocyte stimulator), a non-myelin-associated protein, as a functional ligand for Nogo-66 receptor. J Neurosci 2009;29:6348-6352.PubMedCrossRef
25.
26.
Zurück zum Zitat Mihalcik SA, Huddleston PM, 3rd, Wu X, Jelinek DF. The structure of the TNFRSF13C promoter enables differential expression of BAFF-R during B cell ontogeny and terminal differentiation. J Immunol 2010;185:1045-1054.PubMedPubMedCentralCrossRef Mihalcik SA, Huddleston PM, 3rd, Wu X, Jelinek DF. The structure of the TNFRSF13C promoter enables differential expression of BAFF-R during B cell ontogeny and terminal differentiation. J Immunol 2010;185:1045-1054.PubMedPubMedCentralCrossRef
27.
Zurück zum Zitat Yan M, Brady JR, Chan B, et al. Identification of a novel receptor for B lymphocyte stimulator that is mutated in a mouse strain with severe B cell deficiency. Curr Biol 2001;11:1547-1552.PubMedCrossRef Yan M, Brady JR, Chan B, et al. Identification of a novel receptor for B lymphocyte stimulator that is mutated in a mouse strain with severe B cell deficiency. Curr Biol 2001;11:1547-1552.PubMedCrossRef
28.
Zurück zum Zitat Lougaris V, Gallizzi R, Vitali M, et al. A novel compound heterozygous TACI mutation in an autosomal recessive common variable immunodeficiency (CVID) family. Hum Immunol 2012;73:836-839.PubMedCrossRef Lougaris V, Gallizzi R, Vitali M, et al. A novel compound heterozygous TACI mutation in an autosomal recessive common variable immunodeficiency (CVID) family. Hum Immunol 2012;73:836-839.PubMedCrossRef
29.
Zurück zum Zitat Martinez-Gallo M, Radigan L, Almejun MB, Martinez-Pomar N, Matamoros N, Cunningham-Rundles C. TACI mutations and impaired B-cell function in subjects with CVID and healthy heterozygotes. J Allergy Clin Immunol 2013;131:468-476.PubMedCrossRef Martinez-Gallo M, Radigan L, Almejun MB, Martinez-Pomar N, Matamoros N, Cunningham-Rundles C. TACI mutations and impaired B-cell function in subjects with CVID and healthy heterozygotes. J Allergy Clin Immunol 2013;131:468-476.PubMedCrossRef
30.
Zurück zum Zitat O’Connor BP, Raman VS, Erickson LD, et al. BCMA is essential for the survival of long-lived bone marrow plasma cells. J Exp Med 2004;199:91-98.PubMedPubMedCentralCrossRef O’Connor BP, Raman VS, Erickson LD, et al. BCMA is essential for the survival of long-lived bone marrow plasma cells. J Exp Med 2004;199:91-98.PubMedPubMedCentralCrossRef
31.
Zurück zum Zitat Rosser EC, Mauri C. Regulatory B cells: origin, phenotype, and function. Immunity 2015;42:607-612.PubMedCrossRef Rosser EC, Mauri C. Regulatory B cells: origin, phenotype, and function. Immunity 2015;42:607-612.PubMedCrossRef
32.
Zurück zum Zitat van de Veen W, Stanic B, Yaman G, et al. IgG4 production is confined to human IL-10-producing regulatory B cells that suppress antigen-specific immune responses. J Allergy Clin Immunol 2013;131:1204-1212.PubMedCrossRef van de Veen W, Stanic B, Yaman G, et al. IgG4 production is confined to human IL-10-producing regulatory B cells that suppress antigen-specific immune responses. J Allergy Clin Immunol 2013;131:1204-1212.PubMedCrossRef
34.
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
35.
Zurück zum Zitat Shen P, Roch T, Lampropoulou V, et al. IL-35-producing B cells are critical regulators of immunity during autoimmune and infectious diseases. Nature 2014;507:366-370.PubMedPubMedCentralCrossRef Shen P, Roch T, Lampropoulou V, et al. IL-35-producing B cells are critical regulators of immunity during autoimmune and infectious diseases. Nature 2014;507:366-370.PubMedPubMedCentralCrossRef
36.
Zurück zum Zitat Iwata Y, Matsushita T, Horikawa M, et al. Characterization of a rare IL-10-competent B-cell subset in humans that parallels mouse regulatory B10 cells. Blood 2011;117:530-541.PubMedPubMedCentralCrossRef Iwata Y, Matsushita T, Horikawa M, et al. Characterization of a rare IL-10-competent B-cell subset in humans that parallels mouse regulatory B10 cells. Blood 2011;117:530-541.PubMedPubMedCentralCrossRef
37.
Zurück zum Zitat Miyagaki T, Fujimoto M, Sato S. Regulatory B cells in human inflammatory and autoimmune diseases: from mouse models to clinical research. Int Immunol 2015;27:495-504.PubMedCrossRef Miyagaki T, Fujimoto M, Sato S. Regulatory B cells in human inflammatory and autoimmune diseases: from mouse models to clinical research. Int Immunol 2015;27:495-504.PubMedCrossRef
38.
Zurück zum Zitat Tussiwand R, Bosco N, Ceredig R, Rolink AG. Tolerance checkpoints in B-cell development: Johnny B good. Eur J Immunol 2009;39:2317-2324.PubMedCrossRef Tussiwand R, Bosco N, Ceredig R, Rolink AG. Tolerance checkpoints in B-cell development: Johnny B good. Eur J Immunol 2009;39:2317-2324.PubMedCrossRef
39.
Zurück zum Zitat Dalakas MC. B cells as therapeutic targets in autoimmune neurological disorders. Nat Clin Pract Neurol 2008;4:557-567.PubMedCrossRef Dalakas MC. B cells as therapeutic targets in autoimmune neurological disorders. Nat Clin Pract Neurol 2008;4:557-567.PubMedCrossRef
40.
Zurück zum Zitat Frischer JM, Bramow S, Dal-Bianco A, et al. The relation between inflammation and neurodegeneration in multiple sclerosis brains. Brain 2009;132:1175-1189.PubMedPubMedCentralCrossRef Frischer JM, Bramow S, Dal-Bianco A, et al. The relation between inflammation and neurodegeneration in multiple sclerosis brains. Brain 2009;132:1175-1189.PubMedPubMedCentralCrossRef
41.
Zurück zum Zitat Ozawa K, Suchanek G, Breitschopf H, et al. Patterns of oligodendroglia pathology in multiple sclerosis. Brain 1994;117:1311-1322.PubMedCrossRef Ozawa K, Suchanek G, Breitschopf H, et al. Patterns of oligodendroglia pathology in multiple sclerosis. Brain 1994;117:1311-1322.PubMedCrossRef
42.
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
43.
Zurück zum Zitat Corcione A, Casazza S, Ferretti E, et al. Recapitulation of B cell differentiation in the central nervous system of patients with multiple sclerosis. Proc Natl Acad Sci U S A 2004;101:11064-11069.PubMedPubMedCentralCrossRef Corcione A, Casazza S, Ferretti E, et al. Recapitulation of B cell differentiation in the central nervous system of patients with multiple sclerosis. Proc Natl Acad Sci U S A 2004;101:11064-11069.PubMedPubMedCentralCrossRef
44.
Zurück zum Zitat Harp CT, Ireland S, Davis LS, et al. Memory B cells from a subset of treatment-naive relapsing-remitting multiple sclerosis patients elicit CD4(+) T-cell proliferation and IFN-gamma production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Eur J Immunol 2010;40:2942-2956.PubMedPubMedCentralCrossRef Harp CT, Ireland S, Davis LS, et al. Memory B cells from a subset of treatment-naive relapsing-remitting multiple sclerosis patients elicit CD4(+) T-cell proliferation and IFN-gamma production in response to myelin basic protein and myelin oligodendrocyte glycoprotein. Eur J Immunol 2010;40:2942-2956.PubMedPubMedCentralCrossRef
45.
Zurück zum Zitat Niino M, Hirotani M, Miyazaki Y, Sasaki H. Memory and naive B-cell subsets in patients with multiple sclerosis. Neurosci Lett 2009;464:74-78.PubMedCrossRef Niino M, Hirotani M, Miyazaki Y, Sasaki H. Memory and naive B-cell subsets in patients with multiple sclerosis. Neurosci Lett 2009;464:74-78.PubMedCrossRef
46.
Zurück zum Zitat Habib J, Deng J, Lava N, Tyor W, Galipeau J. Blood B cell and regulatory subset content in multiple sclerosis patients. J Mult Scler (Foster City) 2015;2. Habib J, Deng J, Lava N, Tyor W, Galipeau J. Blood B cell and regulatory subset content in multiple sclerosis patients. J Mult Scler (Foster City) 2015;2.
47.
Zurück zum Zitat Knippenberg S, Peelen E, Smolders J, et al. Reduction in IL-10 producing B cells (Breg) in multiple sclerosis is accompanied by a reduced naive/memory Breg ratio during a relapse but not in remission. J Neuroimmunol 2011;239:80-86.PubMedCrossRef Knippenberg S, Peelen E, Smolders J, et al. Reduction in IL-10 producing B cells (Breg) in multiple sclerosis is accompanied by a reduced naive/memory Breg ratio during a relapse but not in remission. J Neuroimmunol 2011;239:80-86.PubMedCrossRef
48.
Zurück zum Zitat Michel L, Chesneau M, Manceau P, et al. Unaltered regulatory B-cell frequency and function in patients with multiple sclerosis. Clin Immunol 2014;155:198-208.PubMedCrossRef Michel L, Chesneau M, Manceau P, et al. Unaltered regulatory B-cell frequency and function in patients with multiple sclerosis. Clin Immunol 2014;155:198-208.PubMedCrossRef
49.
Zurück zum Zitat Quan C, Yu H, Qiao J, et al. Impaired regulatory function and enhanced intrathecal activation of B cells in neuromyelitis optica: distinct from multiple sclerosis. Mult Scler 2013;19:289-298.PubMedCrossRef Quan C, Yu H, Qiao J, et al. Impaired regulatory function and enhanced intrathecal activation of B cells in neuromyelitis optica: distinct from multiple sclerosis. Mult Scler 2013;19:289-298.PubMedCrossRef
50.
Zurück zum Zitat Hirotani M, Niino M, Fukazawa T, et al. Decreased IL-10 production mediated by Toll-like receptor 9 in B cells in multiple sclerosis. J Neuroimmunol 2010;221:95-100.PubMedCrossRef Hirotani M, Niino M, Fukazawa T, et al. Decreased IL-10 production mediated by Toll-like receptor 9 in B cells in multiple sclerosis. J Neuroimmunol 2010;221:95-100.PubMedCrossRef
51.
Zurück zum Zitat Quan C, ZhangBao J, Lu J, et al. The immune balance between memory and regulatory B cells in NMO and the changes of the balance after methylprednisolone or rituximab therapy. J Neuroimmunol 2015;282:45-53.PubMedCrossRef Quan C, ZhangBao J, Lu J, et al. The immune balance between memory and regulatory B cells in NMO and the changes of the balance after methylprednisolone or rituximab therapy. J Neuroimmunol 2015;282:45-53.PubMedCrossRef
52.
Zurück zum Zitat Myers KJ, Sprent J, Dougherty JP, Ron Y. Synergy between encephalitogenic T cells and myelin basic protein-specific antibodies in the induction of experimental autoimmune encephalomyelitis. J Neuroimmunol 1992;41:1-8.PubMedCrossRef Myers KJ, Sprent J, Dougherty JP, Ron Y. Synergy between encephalitogenic T cells and myelin basic protein-specific antibodies in the induction of experimental autoimmune encephalomyelitis. J Neuroimmunol 1992;41:1-8.PubMedCrossRef
53.
Zurück zum Zitat Willenborg DO, Prowse SJ. Immunoglobulin-deficient rats fail to develop experimental allergic encephalomyelitis. J Neuroimmunol 1983;5:99-109.PubMedCrossRef Willenborg DO, Prowse SJ. Immunoglobulin-deficient rats fail to develop experimental allergic encephalomyelitis. J Neuroimmunol 1983;5:99-109.PubMedCrossRef
54.
Zurück zum Zitat Matsushita T, Horikawa M, Iwata Y, Tedder TF. Regulatory B cells (B10 cells) and regulatory T cells have independent roles in controlling experimental autoimmune encephalomyelitis initiation and late-phase immunopathogenesis. J Immunol 2010;185:2240-2252.PubMedPubMedCentralCrossRef Matsushita T, Horikawa M, Iwata Y, Tedder TF. Regulatory B cells (B10 cells) and regulatory T cells have independent roles in controlling experimental autoimmune encephalomyelitis initiation and late-phase immunopathogenesis. J Immunol 2010;185:2240-2252.PubMedPubMedCentralCrossRef
55.
Zurück zum Zitat Brilot F, Dale RC, Selter RC, et al. Antibodies to native myelin oligodendrocyte glycoprotein in children with inflammatory demyelinating central nervous system disease. Ann Neurol 2009;66:833-842.PubMedCrossRef Brilot F, Dale RC, Selter RC, et al. Antibodies to native myelin oligodendrocyte glycoprotein in children with inflammatory demyelinating central nervous system disease. Ann Neurol 2009;66:833-842.PubMedCrossRef
56.
Zurück zum Zitat Chalmoukou K, Alexopoulos H, Akrivou S, Stathopoulos P, Reindl M, Dalakas MC. Anti-MOG antibodies are frequently associated with steroid-sensitive recurrent optic neuritis. Neurol Neuroimmunol Neuroinflamm 2015;2:e131.PubMedPubMedCentralCrossRef Chalmoukou K, Alexopoulos H, Akrivou S, Stathopoulos P, Reindl M, Dalakas MC. Anti-MOG antibodies are frequently associated with steroid-sensitive recurrent optic neuritis. Neurol Neuroimmunol Neuroinflamm 2015;2:e131.PubMedPubMedCentralCrossRef
57.
Zurück zum Zitat Waters P, Woodhall M, O’Connor KC, et al. MOG cell-based assay detects non-MS patients with inflammatory neurologic disease. Neurol Neuroimmunol Neuroinflamm 2015;2:e89.PubMedCrossRefPubMedCentral Waters P, Woodhall M, O’Connor KC, et al. MOG cell-based assay detects non-MS patients with inflammatory neurologic disease. Neurol Neuroimmunol Neuroinflamm 2015;2:e89.PubMedCrossRefPubMedCentral
58.
Zurück zum Zitat Wang H, Wang K, Zhong X, et al. Cerebrospinal fluid BAFF and APRIL levels in neuromyelitis optica and multiple sclerosis patients during relapse. J Clin Immunol 2012;32:1007-1011.PubMedCrossRef Wang H, Wang K, Zhong X, et al. Cerebrospinal fluid BAFF and APRIL levels in neuromyelitis optica and multiple sclerosis patients during relapse. J Clin Immunol 2012;32:1007-1011.PubMedCrossRef
59.
Zurück zum Zitat Krumbholz M, Faber H, Steinmeyer F, et al. Interferon-beta increases BAFF levels in multiple sclerosis: implications for B cell autoimmunity. Brain 2008;131:1455-1463.PubMedCrossRef Krumbholz M, Faber H, Steinmeyer F, et al. Interferon-beta increases BAFF levels in multiple sclerosis: implications for B cell autoimmunity. Brain 2008;131:1455-1463.PubMedCrossRef
60.
Zurück zum Zitat Krumbholz M, Theil D, Derfuss T, et al. BAFF is produced by astrocytes and up-regulated in multiple sclerosis lesions and primary central nervous system lymphoma. J Exp Med 2005;201:195-200.PubMedPubMedCentralCrossRef Krumbholz M, Theil D, Derfuss T, et al. BAFF is produced by astrocytes and up-regulated in multiple sclerosis lesions and primary central nervous system lymphoma. J Exp Med 2005;201:195-200.PubMedPubMedCentralCrossRef
61.
Zurück zum Zitat Kim SH, Kim W, Li XF, Jung IJ, Kim HJ. Repeated treatment with rituximab based on the assessment of peripheral circulating memory B cells in patients with relapsing neuromyelitis optica over 2 years. Arch Neurol 2011;68:1412-1420.PubMedCrossRef Kim SH, Kim W, Li XF, Jung IJ, Kim HJ. Repeated treatment with rituximab based on the assessment of peripheral circulating memory B cells in patients with relapsing neuromyelitis optica over 2 years. Arch Neurol 2011;68:1412-1420.PubMedCrossRef
62.
Zurück zum Zitat Pellkofer HL, Krumbholz M, Berthele A, et al. Long-term follow-up of patients with neuromyelitis optica after repeated therapy with rituximab. Neurol 2011;76:1310-1315.CrossRef Pellkofer HL, Krumbholz M, Berthele A, et al. Long-term follow-up of patients with neuromyelitis optica after repeated therapy with rituximab. Neurol 2011;76:1310-1315.CrossRef
63.
Zurück zum Zitat Radaelli M, Moiola L, Sangalli F, et al. Neuromyelitis optica spectrum disorders: long-term safety and efficacy of rituximab in Caucasian patients. Mult Scler 2015. Radaelli M, Moiola L, Sangalli F, et al. Neuromyelitis optica spectrum disorders: long-term safety and efficacy of rituximab in Caucasian patients. Mult Scler 2015.
64.
Zurück zum Zitat Satoh J, Onoue H, Arima K, Yamamura T. Nogo-A and nogo receptor expression in demyelinating lesions of multiple sclerosis. J Neuropathol Exp Neurol 2005;64:129-138.PubMedCrossRef Satoh J, Onoue H, Arima K, Yamamura T. Nogo-A and nogo receptor expression in demyelinating lesions of multiple sclerosis. J Neuropathol Exp Neurol 2005;64:129-138.PubMedCrossRef
65.
Zurück zum Zitat Dalakas MC. Autoimmune peripheral neuropathies. In: Rich RR, Fleisher TA, Shearer WT (eds.). Clinical immunology: principles and practice. Philadelphia, PA: Mosby Elsevier, 2011, pp. 977-994. Dalakas MC. Autoimmune peripheral neuropathies. In: Rich RR, Fleisher TA, Shearer WT (eds.). Clinical immunology: principles and practice. Philadelphia, PA: Mosby Elsevier, 2011, pp. 977-994.
66.
Zurück zum Zitat Kusunoki S, Kaida K. Antibodies against ganglioside complexes in Guillain-Barre syndrome and related disorders. J Neurochem 2011;116:828-832.PubMedCrossRef Kusunoki S, Kaida K. Antibodies against ganglioside complexes in Guillain-Barre syndrome and related disorders. J Neurochem 2011;116:828-832.PubMedCrossRef
67.
Zurück zum Zitat Willison HJ, Yuki N. Peripheral neuropathies and anti-glycolipid antibodies. Brain 2002;125:2591-2625.PubMedCrossRef Willison HJ, Yuki N. Peripheral neuropathies and anti-glycolipid antibodies. Brain 2002;125:2591-2625.PubMedCrossRef
69.
Zurück zum Zitat Dalakas MC. Advances in the diagnosis, pathogenesis and treatment of CIDP. Nat Rev Neurol 2011;7:507-517.PubMedCrossRef Dalakas MC. Advances in the diagnosis, pathogenesis and treatment of CIDP. Nat Rev Neurol 2011;7:507-517.PubMedCrossRef
70.
Zurück zum Zitat Dalakas MC, Engel WK. Immunoglobulin and complement deposits in nerves of patients with chronic relapsing polyneuropathy. Arch Neurol 1980;37:637-640.PubMedCrossRef Dalakas MC, Engel WK. Immunoglobulin and complement deposits in nerves of patients with chronic relapsing polyneuropathy. Arch Neurol 1980;37:637-640.PubMedCrossRef
71.
Zurück zum Zitat Dalakas MC, Houff SA, Engel WK, Madden DL, Sever JL. CSF “monoclonal” bands in chronic relapsing polyneuropathy. Neurology 1980;30:864-867.PubMedCrossRef Dalakas MC, Houff SA, Engel WK, Madden DL, Sever JL. CSF “monoclonal” bands in chronic relapsing polyneuropathy. Neurology 1980;30:864-867.PubMedCrossRef
72.
Zurück zum Zitat Stathopoulos P, Alexopoulos H, Dalakas MC. Autoimmune antigenic targets at the node of Ranvier in demyelinating disorders. Nat Rev Neurol 2015;11:143-156.PubMedCrossRef Stathopoulos P, Alexopoulos H, Dalakas MC. Autoimmune antigenic targets at the node of Ranvier in demyelinating disorders. Nat Rev Neurol 2015;11:143-156.PubMedCrossRef
73.
Zurück zum Zitat Tackenberg B, Jelcic I, Baerenwaldt A, et al. Impaired inhibitory Fcγ receptor IIB expression on B cells in chronic inflammatory demyelinating polyneuropathy. Proc Natl Acad Sci U S A 2009;106:4788-4792.PubMedPubMedCentralCrossRef Tackenberg B, Jelcic I, Baerenwaldt A, et al. Impaired inhibitory Fcγ receptor IIB expression on B cells in chronic inflammatory demyelinating polyneuropathy. Proc Natl Acad Sci U S A 2009;106:4788-4792.PubMedPubMedCentralCrossRef
74.
Zurück zum Zitat Ritter C, Forster D, Albrecht P, Hartung HP, Kieseier BC, Lehmann HC. IVIG regulates BAFF expression in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). J Neuroimmunol 2014;274:225-229.PubMedCrossRef Ritter C, Forster D, Albrecht P, Hartung HP, Kieseier BC, Lehmann HC. IVIG regulates BAFF expression in patients with chronic inflammatory demyelinating polyneuropathy (CIDP). J Neuroimmunol 2014;274:225-229.PubMedCrossRef
75.
Zurück zum Zitat Monaco S, Bonetti B, Ferrari S, et al. Complement-mediated demyelination in patients with IgM monoclonal gammopathy and polyneuropathy. N Engl J Med 1990;322:649-652.PubMedCrossRef Monaco S, Bonetti B, Ferrari S, et al. Complement-mediated demyelination in patients with IgM monoclonal gammopathy and polyneuropathy. N Engl J Med 1990;322:649-652.PubMedCrossRef
76.
Zurück zum Zitat Lombardi R, Erne B, Lauria G, et al. IgM deposits on skin nerves in anti-myelin-associated glycoprotein neuropathy. Ann Neurol 2005;57:180-187.PubMedCrossRef Lombardi R, Erne B, Lauria G, et al. IgM deposits on skin nerves in anti-myelin-associated glycoprotein neuropathy. Ann Neurol 2005;57:180-187.PubMedCrossRef
77.
Zurück zum Zitat Campagnolo M, Ferrari S, Dalla Torre C, et al. Polyneuropathy with anti-sulfatide and anti-MAG antibodies: clinical, neurophysiological, pathological features and response to treatment. J Neuroimmunol 2015;281:1-4.PubMedCrossRef Campagnolo M, Ferrari S, Dalla Torre C, et al. Polyneuropathy with anti-sulfatide and anti-MAG antibodies: clinical, neurophysiological, pathological features and response to treatment. J Neuroimmunol 2015;281:1-4.PubMedCrossRef
78.
Zurück zum Zitat Dalakas MC, Rakocevic G, Salajegheh M, et al. Placebo-controlled trial of rituximab in IgM anti-myelin-associated glycoprotein antibody demyelinating neuropathy. Ann Neurol 2009;65:286-293.PubMedCrossRef Dalakas MC, Rakocevic G, Salajegheh M, et al. Placebo-controlled trial of rituximab in IgM anti-myelin-associated glycoprotein antibody demyelinating neuropathy. Ann Neurol 2009;65:286-293.PubMedCrossRef
79.
Zurück zum Zitat Maurer MA, Rakocevic G, Leung CS, et al. Rituximab induces sustained reduction of pathogenic B cells in patients with peripheral nervous system autoimmunity. J Clin Invest 2012;122:1393-1402.PubMedPubMedCentralCrossRef Maurer MA, Rakocevic G, Leung CS, et al. Rituximab induces sustained reduction of pathogenic B cells in patients with peripheral nervous system autoimmunity. J Clin Invest 2012;122:1393-1402.PubMedPubMedCentralCrossRef
80.
Zurück zum Zitat Rizzi M, Knoth R, Hampe CS, et al. Long-lived plasma cells and memory B cells produce pathogenic anti-GAD65 autoantibodies in Stiff Person Syndrome. PLoS One 2010;5:e10838.PubMedPubMedCentralCrossRef Rizzi M, Knoth R, Hampe CS, et al. Long-lived plasma cells and memory B cells produce pathogenic anti-GAD65 autoantibodies in Stiff Person Syndrome. PLoS One 2010;5:e10838.PubMedPubMedCentralCrossRef
81.
Zurück zum Zitat Dalakas MC, Li M, Fujii M, Jacobowitz DM. Stiff person syndrome: quantification, specificity, and intrathecal synthesis of GAD65 antibodies. Neurology 2001;57:780-784.PubMedCrossRef Dalakas MC, Li M, Fujii M, Jacobowitz DM. Stiff person syndrome: quantification, specificity, and intrathecal synthesis of GAD65 antibodies. Neurology 2001;57:780-784.PubMedCrossRef
82.
Zurück zum Zitat Geis C, Weishaupt A, Hallermann S, et al. Stiff person syndrome-associated autoantibodies to amphiphysin mediate reduced GABAergic inhibition. Brain 2010;133:3166-3180.PubMedCrossRef Geis C, Weishaupt A, Hallermann S, et al. Stiff person syndrome-associated autoantibodies to amphiphysin mediate reduced GABAergic inhibition. Brain 2010;133:3166-3180.PubMedCrossRef
83.
Zurück zum Zitat Cohen-Kaminsky S, Delattre RM, Devergne O, et al. High IL-6 gene expression and production by cultured human thymic epithelial cells from patients with myasthenia gravis. Ann N Y Acad Sci 1993;681:97-99.PubMedCrossRef Cohen-Kaminsky S, Delattre RM, Devergne O, et al. High IL-6 gene expression and production by cultured human thymic epithelial cells from patients with myasthenia gravis. Ann N Y Acad Sci 1993;681:97-99.PubMedCrossRef
84.
Zurück zum Zitat Huang D, Pirskanen R, Hjelmstrom P, Lefvert AK. Polymorphisms in IL-1beta and IL-1 receptor antagonist genes are associated with myasthenia gravis. J Neuroimmunol 1998;81:76-81.PubMedCrossRef Huang D, Pirskanen R, Hjelmstrom P, Lefvert AK. Polymorphisms in IL-1beta and IL-1 receptor antagonist genes are associated with myasthenia gravis. J Neuroimmunol 1998;81:76-81.PubMedCrossRef
85.
Zurück zum Zitat Huang YM, Kivisakk P, Ozenci V, Pirskanen R, Link H. Increased levels of circulating acetylcholine receptor (AChR)-reactive IL-10-secreting cells are characteristic for myasthenia gravis (MG). Clin Exp Immunol 1999;118:304-308.PubMedPubMedCentralCrossRef Huang YM, Kivisakk P, Ozenci V, Pirskanen R, Link H. Increased levels of circulating acetylcholine receptor (AChR)-reactive IL-10-secreting cells are characteristic for myasthenia gravis (MG). Clin Exp Immunol 1999;118:304-308.PubMedPubMedCentralCrossRef
86.
Zurück zum Zitat Ragheb S, Lisak R, Lewis R, Van Stavern G, Gonzales F, Simon K. A potential role for B-cell activating factor in the pathogenesis of autoimmune myasthenia gravis. Arch Neurol 2008;65:1358-1362.PubMedCrossRef Ragheb S, Lisak R, Lewis R, Van Stavern G, Gonzales F, Simon K. A potential role for B-cell activating factor in the pathogenesis of autoimmune myasthenia gravis. Arch Neurol 2008;65:1358-1362.PubMedCrossRef
87.
Zurück zum Zitat Dalakas MC. Inflammatory myopathies: management of steroid resistance. Curr Opin Neurol 2011;24:457-462.PubMedCrossRef Dalakas MC. Inflammatory myopathies: management of steroid resistance. Curr Opin Neurol 2011;24:457-462.PubMedCrossRef
88.
Zurück zum Zitat Greenberg SA, Pinkus GS, Amato AA, Pinkus JL. Myeloid dendritic cells in inclusion-body myositis and polymyositis. Muscle Nerve 2007;35:17-23.PubMedCrossRef Greenberg SA, Pinkus GS, Amato AA, Pinkus JL. Myeloid dendritic cells in inclusion-body myositis and polymyositis. Muscle Nerve 2007;35:17-23.PubMedCrossRef
89.
Zurück zum Zitat Salajegheh M, Kong SW, Pinkus JL, et al. Interferon-stimulated gene 15 (ISG15) conjugates proteins in dermatomyositis muscle with perifascicular atrophy. Ann Neurol 2010;67:53-63.PubMedPubMedCentralCrossRef Salajegheh M, Kong SW, Pinkus JL, et al. Interferon-stimulated gene 15 (ISG15) conjugates proteins in dermatomyositis muscle with perifascicular atrophy. Ann Neurol 2010;67:53-63.PubMedPubMedCentralCrossRef
91.
Zurück zum Zitat Aggarwal R, Bandos A, Reed AM, et al. Predictors of clinical improvement in rituximab-treated refractory adult and juvenile dermatomyositis and adult polymyositis. Arthritis Rheumatol 2014;66:740-749.PubMedPubMedCentralCrossRef Aggarwal R, Bandos A, Reed AM, et al. Predictors of clinical improvement in rituximab-treated refractory adult and juvenile dermatomyositis and adult polymyositis. Arthritis Rheumatol 2014;66:740-749.PubMedPubMedCentralCrossRef
92.
Zurück zum Zitat Chung L, Genovese MC, Fiorentino DF. A pilot trial of rituximab in the treatment of patients with dermatomyositis. Arch Dermatol 2007;143:763-767.PubMedCrossRef Chung L, Genovese MC, Fiorentino DF. A pilot trial of rituximab in the treatment of patients with dermatomyositis. Arch Dermatol 2007;143:763-767.PubMedCrossRef
93.
Zurück zum Zitat Haroon M, Devlin J. Rituximab as a first-line agent for the treatment of dermatomyositis. Rheumatol Int 2012;32:1783-1784.PubMedCrossRef Haroon M, Devlin J. Rituximab as a first-line agent for the treatment of dermatomyositis. Rheumatol Int 2012;32:1783-1784.PubMedCrossRef
94.
Zurück zum Zitat Levine TD. Rituximab in the treatment of dermatomyositis: an open-label pilot study. Arthritis Rheum 2005;52:601-607.PubMedCrossRef Levine TD. Rituximab in the treatment of dermatomyositis: an open-label pilot study. Arthritis Rheum 2005;52:601-607.PubMedCrossRef
95.
Zurück zum Zitat Rios Fernandez R, Callejas Rubio JL, Sanchez Cano D, Saez Moreno JA, Ortego Centeno N. Rituximab in the treatment of dermatomyositis and other inflammatory myopathies. A report of 4 cases and review of the literature. Clin Exp Rheumatol 2009;27:1009-1016.PubMed Rios Fernandez R, Callejas Rubio JL, Sanchez Cano D, Saez Moreno JA, Ortego Centeno N. Rituximab in the treatment of dermatomyositis and other inflammatory myopathies. A report of 4 cases and review of the literature. Clin Exp Rheumatol 2009;27:1009-1016.PubMed
96.
Zurück zum Zitat Leone A, Sciascia S, Kamal A, Khamashta M. Biologicals for the treatment of systemic lupus erythematosus: current status and emerging therapies. Exp Rev Clin Immunol 2015;11:109-116.CrossRef Leone A, Sciascia S, Kamal A, Khamashta M. Biologicals for the treatment of systemic lupus erythematosus: current status and emerging therapies. Exp Rev Clin Immunol 2015;11:109-116.CrossRef
97.
Zurück zum Zitat Luhder F, Gold R. Trial and error in clinical studies: lessons from ATAMS. Lancet Neurol 2014;13:340-341.PubMedCrossRef Luhder F, Gold R. Trial and error in clinical studies: lessons from ATAMS. Lancet Neurol 2014;13:340-341.PubMedCrossRef
98.
Zurück zum Zitat Fujimoto M, Poe JC, Hasegawa M, Tedder TF. CD19 regulates intrinsic B lymphocyte signal transduction and activation through a novel mechanism of processive amplification. Immunol Res 2000;22:281-298.PubMedCrossRef Fujimoto M, Poe JC, Hasegawa M, Tedder TF. CD19 regulates intrinsic B lymphocyte signal transduction and activation through a novel mechanism of processive amplification. Immunol Res 2000;22:281-298.PubMedCrossRef
99.
Zurück zum Zitat Herbst R, Wang Y, Gallagher S, et al. B-cell depletion in vitro and in vivo with an afucosylated anti-CD19 antibody. J Pharmacol Exp Ther 2010;335:213-222.PubMedCrossRef Herbst R, Wang Y, Gallagher S, et al. B-cell depletion in vitro and in vivo with an afucosylated anti-CD19 antibody. J Pharmacol Exp Ther 2010;335:213-222.PubMedCrossRef
100.
Zurück zum Zitat Tedder TF, Poe JC, Haas KM. CD22: a multifunctional receptor that regulates B lymphocyte survival and signal transduction. Adv Immunol 2005;88:1-50.PubMedCrossRef Tedder TF, Poe JC, Haas KM. CD22: a multifunctional receptor that regulates B lymphocyte survival and signal transduction. Adv Immunol 2005;88:1-50.PubMedCrossRef
101.
Zurück zum Zitat Goede V, Klein C, Stilgenbauer S. Obinutuzumab (GA101) for the treatment of chronic lymphocytic leukemia and other B-cell non-hodgkin’s lymphomas: a glycoengineered type II CD20 antibody. Oncol Res Treat 2015;38:185-192.PubMedCrossRef Goede V, Klein C, Stilgenbauer S. Obinutuzumab (GA101) for the treatment of chronic lymphocytic leukemia and other B-cell non-hodgkin’s lymphomas: a glycoengineered type II CD20 antibody. Oncol Res Treat 2015;38:185-192.PubMedCrossRef
102.
Zurück zum Zitat Robak P, Smolewski P, Robak T. Emerging immunological drugs for chronic lymphocytic leukemia. Exp Opin Emerg Drugs 2015;20:423-447.CrossRef Robak P, Smolewski P, Robak T. Emerging immunological drugs for chronic lymphocytic leukemia. Exp Opin Emerg Drugs 2015;20:423-447.CrossRef
103.
Zurück zum Zitat Teo EC, Chew Y, Phipps C. A review of monoclonal antibody therapies in lymphoma. Crit Rev Oncol Hematol 2015. Teo EC, Chew Y, Phipps C. A review of monoclonal antibody therapies in lymphoma. Crit Rev Oncol Hematol 2015.
104.
Zurück zum Zitat Palanichamy A, Jahn S, Nickles D, et al. Rituximab efficiently depletes increased CD20-expressing T cells in multiple sclerosis patients. J Immunol 2014;193:580-586.PubMedPubMedCentralCrossRef Palanichamy A, Jahn S, Nickles D, et al. Rituximab efficiently depletes increased CD20-expressing T cells in multiple sclerosis patients. J Immunol 2014;193:580-586.PubMedPubMedCentralCrossRef
105.
Zurück zum Zitat Petereit HF, Rubbert-Roth A. Rituximab levels in cerebrospinal fluid of patients with neurological autoimmune disorders. Mult Scler 2009;15:189-192.PubMedCrossRef Petereit HF, Rubbert-Roth A. Rituximab levels in cerebrospinal fluid of patients with neurological autoimmune disorders. Mult Scler 2009;15:189-192.PubMedCrossRef
106.
Zurück zum Zitat Cross AH, Stark JL, Lauber J, Ramsbottom MJ, Lyons JA. Rituximab reduces B cells and T cells in cerebrospinal fluid of multiple sclerosis patients. J Neuroimmunol 2006;180:63-70.PubMedPubMedCentralCrossRef Cross AH, Stark JL, Lauber J, Ramsbottom MJ, Lyons JA. Rituximab reduces B cells and T cells in cerebrospinal fluid of multiple sclerosis patients. J Neuroimmunol 2006;180:63-70.PubMedPubMedCentralCrossRef
107.
Zurück zum Zitat Bar-Or A, Calabresi PA, Arnold D, et al. Rituximab in relapsing-remitting multiple sclerosis: a 72-week, open-label, phase I trial. Ann Neurol 2008;63:395-400PubMedCrossRef Bar-Or A, Calabresi PA, Arnold D, et al. Rituximab in relapsing-remitting multiple sclerosis: a 72-week, open-label, phase I trial. Ann Neurol 2008;63:395-400PubMedCrossRef
108.
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
109.
Zurück zum Zitat Nielsen AS, Miravalle A, Langer-Gould A, Cooper J, Edwards KR, Kinkel RP. Maximally tolerated versus minimally effective dose: the case of rituximab in multiple sclerosis. Mult Scler 2012;18:377-378.PubMedCrossRef Nielsen AS, Miravalle A, Langer-Gould A, Cooper J, Edwards KR, Kinkel RP. Maximally tolerated versus minimally effective dose: the case of rituximab in multiple sclerosis. Mult Scler 2012;18:377-378.PubMedCrossRef
110.
111.
Zurück zum Zitat Evdoshenko E, Maslyanskiy A, Lapin S, et al. Dynamics of B-cell populations in CSF and blood in patients treated with a combination of rituximab and mitoxantrone. ISRN Neurol 2013;2013:748127.PubMedCrossRefPubMedCentral Evdoshenko E, Maslyanskiy A, Lapin S, et al. Dynamics of B-cell populations in CSF and blood in patients treated with a combination of rituximab and mitoxantrone. ISRN Neurol 2013;2013:748127.PubMedCrossRefPubMedCentral
112.
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
113.
Zurück zum Zitat Bedi GS, Brown AD, Delgado SR, Usmani N, Lam BL, Sheremata WA. Impact of rituximab on relapse rate and disability in neuromyelitis optica. Mult Scler 2011;17:1225-1230.PubMedCrossRef Bedi GS, Brown AD, Delgado SR, Usmani N, Lam BL, Sheremata WA. Impact of rituximab on relapse rate and disability in neuromyelitis optica. Mult Scler 2011;17:1225-1230.PubMedCrossRef
114.
Zurück zum Zitat Cree BA, Lamb S, Morgan K, Chen A, Waubant E, Genain C. An open label study of the effects of rituximab in neuromyelitis optica. Neurology 2005;64:1270-1272.PubMedCrossRef Cree BA, Lamb S, Morgan K, Chen A, Waubant E, Genain C. An open label study of the effects of rituximab in neuromyelitis optica. Neurology 2005;64:1270-1272.PubMedCrossRef
115.
Zurück zum Zitat Ip VH, Lau AY, Au LW, et al. Rituximab reduces attacks in Chinese patients with neuromyelitis optica spectrum disorders. J Neurol Sci 2013;324:38-39.PubMedCrossRef Ip VH, Lau AY, Au LW, et al. Rituximab reduces attacks in Chinese patients with neuromyelitis optica spectrum disorders. J Neurol Sci 2013;324:38-39.PubMedCrossRef
116.
Zurück zum Zitat Jacob A, Weinshenker BG, Violich I, et al. Treatment of neuromyelitis optica with rituximab: retrospective analysis of 25 patients. Arch Neurol 2008;65:1443-1448.PubMedCrossRef Jacob A, Weinshenker BG, Violich I, et al. Treatment of neuromyelitis optica with rituximab: retrospective analysis of 25 patients. Arch Neurol 2008;65:1443-1448.PubMedCrossRef
117.
Zurück zum Zitat Mahmood NA, Silver K, Onel K, Ko M, Javed A. Efficacy and safety of rituximab in pediatric neuromyelitis optica. J Child Neurol 2011;26:244-247.PubMedCrossRef Mahmood NA, Silver K, Onel K, Ko M, Javed A. Efficacy and safety of rituximab in pediatric neuromyelitis optica. J Child Neurol 2011;26:244-247.PubMedCrossRef
118.
Zurück zum Zitat Gredler V, Mader S, Schanda K, et al. Clinical and immunological follow-up of B-cell depleting therapy in CNS demyelinating diseases. J Neurol Sci 2013;328:77-82.PubMedCrossRef Gredler V, Mader S, Schanda K, et al. Clinical and immunological follow-up of B-cell depleting therapy in CNS demyelinating diseases. J Neurol Sci 2013;328:77-82.PubMedCrossRef
119.
Zurück zum Zitat Kim SH, Jeong IH, Hyun JW, 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 SH, Jeong IH, Hyun JW, 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
120.
Zurück zum Zitat Mealy MA, Wingerchuk DM, Palace J, Greenberg BM, Levy M. Comparison of relapse and treatment failure rates among patients with neuromyelitis optica: multicenter study of treatment efficacy. JAMA Neurol 2014;71:324-330.PubMedCrossRef Mealy MA, Wingerchuk DM, Palace J, Greenberg BM, Levy M. Comparison of relapse and treatment failure rates among patients with neuromyelitis optica: multicenter study of treatment efficacy. JAMA Neurol 2014;71:324-330.PubMedCrossRef
121.
Zurück zum Zitat Nakashima I, Takahashi T, Cree BA, et al. Transient increases in anti-aquaporin-4 antibody titers following rituximab treatment in neuromyelitis optica, in association with elevated serum BAFF levels. J Clin Neurosci 2011;18:997-998.PubMedCrossRef Nakashima I, Takahashi T, Cree BA, et al. Transient increases in anti-aquaporin-4 antibody titers following rituximab treatment in neuromyelitis optica, in association with elevated serum BAFF levels. J Clin Neurosci 2011;18:997-998.PubMedCrossRef
122.
Zurück zum Zitat Perumal JS, Kister I, Howard J, Herbert J. Disease exacerbation after rituximab induction in neuromyelitis optica. Neurol Neuroimmunol Neuroinflamm 2015;2:e61.PubMedPubMedCentralCrossRef Perumal JS, Kister I, Howard J, Herbert J. Disease exacerbation after rituximab induction in neuromyelitis optica. Neurol Neuroimmunol Neuroinflamm 2015;2:e61.PubMedPubMedCentralCrossRef
123.
Zurück zum Zitat Karenfort M, Kieseier BC, Tibussek D, Assmann B, Schaper J, Mayatepek E. Rituximab as a highly effective treatment in a female adolescent with severe multiple sclerosis. Develop Med Child Neurol 2009;51:159-161.PubMedCrossRef Karenfort M, Kieseier BC, Tibussek D, Assmann B, Schaper J, Mayatepek E. Rituximab as a highly effective treatment in a female adolescent with severe multiple sclerosis. Develop Med Child Neurol 2009;51:159-161.PubMedCrossRef
124.
Zurück zum Zitat Tzaribachev N, Koetter I, Kuemmerle-Deschner JB, Schedel J. Rituximab for the treatment of refractory pediatric autoimmune diseases: a case series. Cases J 2009;2:6609PubMedPubMedCentralCrossRef Tzaribachev N, Koetter I, Kuemmerle-Deschner JB, Schedel J. Rituximab for the treatment of refractory pediatric autoimmune diseases: a case series. Cases J 2009;2:6609PubMedPubMedCentralCrossRef
125.
Zurück zum Zitat Beres SJ, Graves J, Waubant E. Rituximab use in pediatric central demyelinating disease. Pediatr Neurol 2014;51:114-118.PubMedCrossRef Beres SJ, Graves J, Waubant E. Rituximab use in pediatric central demyelinating disease. Pediatr Neurol 2014;51:114-118.PubMedCrossRef
126.
Zurück zum Zitat Bacorro EA, Tehrani R. Stiff-person syndrome: persistent elevation of glutamic acid decarboxylase antibodies despite successful treatment with rituximab. J Clin Rheumatol 2010;16:237-239.PubMedCrossRef Bacorro EA, Tehrani R. Stiff-person syndrome: persistent elevation of glutamic acid decarboxylase antibodies despite successful treatment with rituximab. J Clin Rheumatol 2010;16:237-239.PubMedCrossRef
127.
Zurück zum Zitat Lobo ME, Araujo ML, Tomaz CA, Allam N. Stiff-person syndrome treated with rituximab. BMJ Case Rep 2010;2010. Lobo ME, Araujo ML, Tomaz CA, Allam N. Stiff-person syndrome treated with rituximab. BMJ Case Rep 2010;2010.
128.
Zurück zum Zitat Dupond JL, Essalmi L, Gil H, Meaux-Ruault N, Hafsaoui C. Rituximab treatment of stiff-person syndrome in a patient with thymoma, diabetes mellitus and autoimmune thyroiditis. J Clin Neurosci 2010;17:389-391.PubMedCrossRef Dupond JL, Essalmi L, Gil H, Meaux-Ruault N, Hafsaoui C. Rituximab treatment of stiff-person syndrome in a patient with thymoma, diabetes mellitus and autoimmune thyroiditis. J Clin Neurosci 2010;17:389-391.PubMedCrossRef
129.
Zurück zum Zitat Katoh N, Matsuda M, Ishii W, Morita H, Ikeda S. Successful treatment with rituximab in a patient with stiff-person syndrome complicated by dysthyroid ophthalmopathy. Intern Med 2010;49:237-241.PubMedCrossRef Katoh N, Matsuda M, Ishii W, Morita H, Ikeda S. Successful treatment with rituximab in a patient with stiff-person syndrome complicated by dysthyroid ophthalmopathy. Intern Med 2010;49:237-241.PubMedCrossRef
130.
Zurück zum Zitat Qureshi A, Hennessy M. Stiff person syndrome (SPS) complicated by respiratory failure: successful treatment with rituximab. J Neurol 2012;259:180-181.PubMedCrossRef Qureshi A, Hennessy M. Stiff person syndrome (SPS) complicated by respiratory failure: successful treatment with rituximab. J Neurol 2012;259:180-181.PubMedCrossRef
131.
Zurück zum Zitat Zdziarski P. A case of stiff person syndrome: immunomodulatory effect of benzodiazepines: successful rituximab and tizanidine therapy. Medicine 2015;94:e954.PubMedPubMedCentralCrossRef Zdziarski P. A case of stiff person syndrome: immunomodulatory effect of benzodiazepines: successful rituximab and tizanidine therapy. Medicine 2015;94:e954.PubMedPubMedCentralCrossRef
132.
Zurück zum Zitat Dalakas MC, Rakocevic G, Dambrosia J, McElroy B. A double-blind, placebo-cotrolled study of rituximab in patients with stiff-person syndrome (SPS). Ann Neurol 2009;66:S20. Dalakas MC, Rakocevic G, Dambrosia J, McElroy B. A double-blind, placebo-cotrolled study of rituximab in patients with stiff-person syndrome (SPS). Ann Neurol 2009;66:S20.
133.
Zurück zum Zitat Nowak RJ, Dicapua DB, Zebardast N, Goldstein JM. Response of patients with refractory myasthenia gravis to rituximab: a retrospective study. Ther Adv Neurol Disord 2011;4:259-266.PubMedPubMedCentralCrossRef Nowak RJ, Dicapua DB, Zebardast N, Goldstein JM. Response of patients with refractory myasthenia gravis to rituximab: a retrospective study. Ther Adv Neurol Disord 2011;4:259-266.PubMedPubMedCentralCrossRef
134.
Zurück zum Zitat Keung B, Robeson KR, DiCapua DB, et al. Long-term benefit of rituximab in MuSK autoantibody myasthenia gravis patients. J Neurol Neurosurg Psychiatry 2013;84:1407-1409.PubMedCrossRef Keung B, Robeson KR, DiCapua DB, et al. Long-term benefit of rituximab in MuSK autoantibody myasthenia gravis patients. J Neurol Neurosurg Psychiatry 2013;84:1407-1409.PubMedCrossRef
135.
Zurück zum Zitat Iorio R, Damato V, Alboini PE, Evoli A. 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, Evoli A. Efficacy and safety of rituximab for myasthenia gravis: a systematic review and meta-analysis. J Neurol 2015;262:1115-1119.PubMedCrossRef
136.
Zurück zum Zitat Oddis CV, Reed AM, Aggarwal R, et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum 2013;65:314-324.PubMedPubMedCentralCrossRef Oddis CV, Reed AM, Aggarwal R, et al. Rituximab in the treatment of refractory adult and juvenile dermatomyositis and adult polymyositis: a randomized, placebo-phase trial. Arthritis Rheum 2013;65:314-324.PubMedPubMedCentralCrossRef
137.
Zurück zum Zitat Martin Mdel P, Cravens PD, Winger R, et al. Depletion of B lymphocytes from cerebral perivascular spaces by rituximab. Arch Neurol 2009;66:1016-1020.PubMed Martin Mdel P, Cravens PD, Winger R, et al. Depletion of B lymphocytes from cerebral perivascular spaces by rituximab. Arch Neurol 2009;66:1016-1020.PubMed
138.
Zurück zum Zitat Carson KR, Focosi D, Major EO, et al. Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. Lancet Oncol 2009;10:816-824.PubMedCrossRef Carson KR, Focosi D, Major EO, et al. Monoclonal antibody-associated progressive multifocal leucoencephalopathy in patients treated with rituximab, natalizumab, and efalizumab: a Review from the Research on Adverse Drug Events and Reports (RADAR) Project. Lancet Oncol 2009;10:816-824.PubMedCrossRef
139.
Zurück zum Zitat De Palma R, Sementa A. Rituximab in relapsing-remitting multiple sclerosis. N Engl J Med 2008;358:2645-2646.PubMedCrossRef De Palma R, Sementa A. Rituximab in relapsing-remitting multiple sclerosis. N Engl J Med 2008;358:2645-2646.PubMedCrossRef
140.
Zurück zum Zitat Shetty S, Ahmed AR. Preliminary analysis of mortality associated with rituximab use in autoimmune diseases. Autoimmunity 2013;46:487-496.PubMedCrossRef Shetty S, Ahmed AR. Preliminary analysis of mortality associated with rituximab use in autoimmune diseases. Autoimmunity 2013;46:487-496.PubMedCrossRef
141.
Zurück zum Zitat Kim SH, Huh SY, Lee SJ, Joung A, Kim HJ. A 5-year follow-up of rituximab treatment in patients with neuromyelitis optica spectrum disorder. JAMA Neurol 2013;70:1110-1117.PubMedCrossRef Kim SH, Huh SY, Lee SJ, Joung A, Kim HJ. A 5-year follow-up of rituximab treatment in patients with neuromyelitis optica spectrum disorder. JAMA Neurol 2013;70:1110-1117.PubMedCrossRef
142.
Zurück zum Zitat Weinfurtner K, Graves J, Ness J, Krupp L, Milazzo M, Waubant E. Prolonged remission in neuromyelitis optica following cessation of rituximab treatment. J Child Neurol 2015;30:1366-1370.PubMedCrossRef Weinfurtner K, Graves J, Ness J, Krupp L, Milazzo M, Waubant E. Prolonged remission in neuromyelitis optica following cessation of rituximab treatment. J Child Neurol 2015;30:1366-1370.PubMedCrossRef
143.
Zurück zum Zitat Svenningsson A, Bergman J, Dring A, et al. Rapid depletion of B lymphocytes by ultra-low-dose rituximab delivered intrathecally. Neurol Neuroimmunol Neuroinflamm 2015;2:e79.PubMedPubMedCentralCrossRef Svenningsson A, Bergman J, Dring A, et al. Rapid depletion of B lymphocytes by ultra-low-dose rituximab delivered intrathecally. Neurol Neuroimmunol Neuroinflamm 2015;2:e79.PubMedPubMedCentralCrossRef
144.
Zurück zum Zitat Marnetto F, Granieri L, Valentino P, Capobianco M, Pautasso M, Bertolotto A. CD19 mRNA quantification improves rituximab treatment-to-target approach: a proof of concept study. J Neuroimmunol 2014;277:127-133.PubMedCrossRef Marnetto F, Granieri L, Valentino P, Capobianco M, Pautasso M, Bertolotto A. CD19 mRNA quantification improves rituximab treatment-to-target approach: a proof of concept study. J Neuroimmunol 2014;277:127-133.PubMedCrossRef
145.
Zurück zum Zitat Stork AC, Notermans NC, van den Berg LH, et al. Fcgamma receptor IIIA genotype is associated with rituximab response in antimyelin-associated glycoprotein neuropathy. J Neurol Neurosurg Psychiatry 2014;85:918-920.PubMedCrossRef Stork AC, Notermans NC, van den Berg LH, et al. Fcgamma receptor IIIA genotype is associated with rituximab response in antimyelin-associated glycoprotein neuropathy. J Neurol Neurosurg Psychiatry 2014;85:918-920.PubMedCrossRef
146.
Zurück zum Zitat Emery P, Rigby W, Tak PP, et al. Safety with ocrelizumab in rheumatoid arthritis: results from the ocrelizumab phase III program. PLoS One 2014;9:e87379.PubMedPubMedCentralCrossRef Emery P, Rigby W, Tak PP, et al. Safety with ocrelizumab in rheumatoid arthritis: results from the ocrelizumab phase III program. PLoS One 2014;9:e87379.PubMedPubMedCentralCrossRef
147.
Zurück zum Zitat Harigai M, Tanaka Y, Maisawa S. Safety and efficacy of various dosages of ocrelizumab in Japanese patients with rheumatoid arthritis with an inadequate response to methotrexate therapy: a placebo-controlled double-blind parallel-group study. J Rheumatol 2012;39:486-495.PubMedCrossRef Harigai M, Tanaka Y, Maisawa S. Safety and efficacy of various dosages of ocrelizumab in Japanese patients with rheumatoid arthritis with an inadequate response to methotrexate therapy: a placebo-controlled double-blind parallel-group study. J Rheumatol 2012;39:486-495.PubMedCrossRef
148.
Zurück zum Zitat Mysler EF, Spindler AJ, Guzman R, et al. Efficacy and safety of ocrelizumab in active proliferative lupus nephritis: results from a randomized, double-blind, phase III study. Arthritis Rheum 2013;65:2368-2379.PubMedCrossRef Mysler EF, Spindler AJ, Guzman R, et al. Efficacy and safety of ocrelizumab in active proliferative lupus nephritis: results from a randomized, double-blind, phase III study. Arthritis Rheum 2013;65:2368-2379.PubMedCrossRef
149.
Zurück zum Zitat Rigby W, Tony HP, 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 Rheum 2012;64:350-359.PubMedCrossRef Rigby W, Tony HP, 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 Rheum 2012;64:350-359.PubMedCrossRef
150.
Zurück zum Zitat Stohl W, Gomez-Reino J, Olech E, et al. Safety and efficacy of ocrelizumab in combination with methotrexate in MTX-naive subjects with rheumatoid arthritis: the phase III FILM trial. Ann Rheum Dis 2012;71:1289-1296.PubMedPubMedCentralCrossRef Stohl W, Gomez-Reino J, Olech E, et al. Safety and efficacy of ocrelizumab in combination with methotrexate in MTX-naive subjects with rheumatoid arthritis: the phase III FILM trial. Ann Rheum Dis 2012;71:1289-1296.PubMedPubMedCentralCrossRef
151.
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 Rheum 2012;64:360-370.PubMedCrossRef 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 Rheum 2012;64:360-370.PubMedCrossRef
152.
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
153.
Zurück zum Zitat Sorensen PS, Lisby S, Grove R, et al. Safety and efficacy of ofatumumab in relapsing-remitting multiple sclerosis: a phase 2 study. Neurology 2014;82:573-581.PubMedCrossRef Sorensen PS, Lisby S, Grove R, et al. Safety and efficacy of ofatumumab in relapsing-remitting multiple sclerosis: a phase 2 study. Neurology 2014;82:573-581.PubMedCrossRef
154.
Zurück zum Zitat Ketterl TG, Messinger YH, Niess DR, Gilles E, Engel WK, Perkins JL. Ofatumumab for refractory opsoclonus-myoclonus syndrome following treatment of neuroblastoma. Pediatr Blood Cancer 2013;60:E163-E165.PubMedCrossRef Ketterl TG, Messinger YH, Niess DR, Gilles E, Engel WK, Perkins JL. Ofatumumab for refractory opsoclonus-myoclonus syndrome following treatment of neuroblastoma. Pediatr Blood Cancer 2013;60:E163-E165.PubMedCrossRef
155.
Zurück zum Zitat Pranzatelli MR, Tate ED, Shenoy S, Travelstead AL. Ofatumumab for a rituximab-allergic child with chronic-relapsing paraneoplastic opsoclonus-myoclonus. Pediatr Blood Cancer 2012;58:988-991.PubMedCrossRef Pranzatelli MR, Tate ED, Shenoy S, Travelstead AL. Ofatumumab for a rituximab-allergic child with chronic-relapsing paraneoplastic opsoclonus-myoclonus. Pediatr Blood Cancer 2012;58:988-991.PubMedCrossRef
Metadaten
Titel
Anti-B-Cell Therapies in Autoimmune Neurological Diseases: Rationale and Efficacy Trials
verfasst von
Harry Alexopoulos
Angie Biba
Marinos C. Dalakas
Publikationsdatum
01.01.2016
Verlag
Springer US
Erschienen in
Neurotherapeutics / Ausgabe 1/2016
Print ISSN: 1933-7213
Elektronische ISSN: 1878-7479
DOI
https://doi.org/10.1007/s13311-015-0402-6

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