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Erschienen in: Journal of Neurology 5/2021

03.09.2019 | Review

Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review

verfasst von: Jayne L. Chamberlain, Saif Huda, Daniel H. Whittam, Marcelo Matiello, B. Paul Morgan, Anu Jacob

Erschienen in: Journal of Neurology | Ausgabe 5/2021

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Abstract

The complement system is a powerful member of the innate immune system. It is highly adept at protecting against pathogens, but exists in a delicate balance between its protective functions and overactivity, which can result in autoimmune disease. A cascade of complement proteins that requires sequential activation, and numerous complement regulators, exists to regulate a proportionate response to pathogens. In spite of these mechanisms there is significant evidence for involvement of the complement system in driving the pathogenesis of variety of diseases including neuromyelitis optica spectrum disorders (NMOSD) and myasthenia gravis (MG). As an amplification cascade, there are an abundance of molecular targets that could be utilized for therapeutic intervention. Clinical trials assessing complement pathway inhibition in both these conditions have recently been completed and include the first randomized placebo-controlled trial in NMOSD showing positive results. This review aims to review and update the reader on the complement system and the evolution of complement-based therapeutics in these two disorders.
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Literatur
2.
Zurück zum Zitat Petersen JG, Dorrington KJ (1974) An in vitro system for studying the kinetics of interchain disulfide bond formation in immunoglobulin G. J Biol Chem 249:5633–5641PubMed Petersen JG, Dorrington KJ (1974) An in vitro system for studying the kinetics of interchain disulfide bond formation in immunoglobulin G. J Biol Chem 249:5633–5641PubMed
3.
Zurück zum Zitat van der Zee JS, van Swieten P, Aalberse RC (1986) Serologic aspects of IgG4 antibodies. II. IgG4 antibodies form small, nonprecipitating immune complexes due to functional monovalency. J Immunol 137:3566–3571PubMed van der Zee JS, van Swieten P, Aalberse RC (1986) Serologic aspects of IgG4 antibodies. II. IgG4 antibodies form small, nonprecipitating immune complexes due to functional monovalency. J Immunol 137:3566–3571PubMed
4.
Zurück zum Zitat Angal S, King DJ, Bodmer MW et al (1993) A single amino acid substitution abolishes the heterogeneity of chimeric mouse/human (IgG4) antibody. Mol Immunol 30:105–108PubMed Angal S, King DJ, Bodmer MW et al (1993) A single amino acid substitution abolishes the heterogeneity of chimeric mouse/human (IgG4) antibody. Mol Immunol 30:105–108PubMed
5.
Zurück zum Zitat Schuurman J, Perdok GJ, Gorter AD, Aalberse RC (2001) The inter-heavy chain disulfide bonds of IgG4 are in equilibrium with intra-chain disulfide bonds. Mol Immunol 38:1–8PubMed Schuurman J, Perdok GJ, Gorter AD, Aalberse RC (2001) The inter-heavy chain disulfide bonds of IgG4 are in equilibrium with intra-chain disulfide bonds. Mol Immunol 38:1–8PubMed
17.
Zurück zum Zitat Grumach AS, Kirschfink M (2014) Are complement deficiencies really rare? Overview on prevalence, clinical importance and modern diagnostic approach. Mol Immunol 61:110–117PubMed Grumach AS, Kirschfink M (2014) Are complement deficiencies really rare? Overview on prevalence, clinical importance and modern diagnostic approach. Mol Immunol 61:110–117PubMed
20.
Zurück zum Zitat Yih Chen J, Ling WuY, Yin Mok M et al (2016) Effects of complement C4 gene copy number variations, size dichotomy, and C4A deficiency on genetic risk and clinical presentation of systemic lupus erythematosus in East Asian populations. Arthritis Rheumatol 68:1442–1453. https://doi.org/10.1002/art.39589CrossRef Yih Chen J, Ling WuY, Yin Mok M et al (2016) Effects of complement C4 gene copy number variations, size dichotomy, and C4A deficiency on genetic risk and clinical presentation of systemic lupus erythematosus in East Asian populations. Arthritis Rheumatol 68:1442–1453. https://​doi.​org/​10.​1002/​art.​39589CrossRef
21.
Zurück zum Zitat Fleming SD, Shea-Donohue T, Guthridge JM et al (2002) Mice deficient in complement receptors 1 and 2 lack a tissue injury-inducing subset of the natural antibody repertoire. J Immunol 169:2126–2133PubMed Fleming SD, Shea-Donohue T, Guthridge JM et al (2002) Mice deficient in complement receptors 1 and 2 lack a tissue injury-inducing subset of the natural antibody repertoire. J Immunol 169:2126–2133PubMed
33.
Zurück zum Zitat Wingerchuk DM, Hogancamp WF, O’Brien PC, Weinshenker BG (1999) The clinical course of neuromyelitis optica (Devic’s syndrome). Neurology 53:1107–1114PubMed Wingerchuk DM, Hogancamp WF, O’Brien PC, Weinshenker BG (1999) The clinical course of neuromyelitis optica (Devic’s syndrome). Neurology 53:1107–1114PubMed
46.
Zurück zum Zitat Lucchinetti CF, Mandler RN, Mcgavern D et al (2002) A role for humoral mechanisms in the pathogenesis of Devic’s neuromyelitis optica. Brain 125:1450–1461PubMed Lucchinetti CF, Mandler RN, Mcgavern D et al (2002) A role for humoral mechanisms in the pathogenesis of Devic’s neuromyelitis optica. Brain 125:1450–1461PubMed
48.
Zurück zum Zitat Lumsden CE (1971) The immunogenesis of the multiple sclerosis plaque. Brain Res 28:365–390PubMed Lumsden CE (1971) The immunogenesis of the multiple sclerosis plaque. Brain Res 28:365–390PubMed
54.
Zurück zum Zitat Brink BP, Veerhuis R, Breij ECW et al (2005) The pathology of multiple sclerosis is location-dependent: no significant complement activation is detected in purely cortical lesions. J Neuropathol Exp Neurol 64:147–155PubMed Brink BP, Veerhuis R, Breij ECW et al (2005) The pathology of multiple sclerosis is location-dependent: no significant complement activation is detected in purely cortical lesions. J Neuropathol Exp Neurol 64:147–155PubMed
55.
Zurück zum Zitat Vamvakas EC, Pineda AA, Weinshenker BG (1995) Meta-analysis of clinical studies of the efficacy of plasma exchange in the treatment of chronic progressive multiple sclerosis. J Clin Apher 10:163–170PubMed Vamvakas EC, Pineda AA, Weinshenker BG (1995) Meta-analysis of clinical studies of the efficacy of plasma exchange in the treatment of chronic progressive multiple sclerosis. J Clin Apher 10:163–170PubMed
56.
Zurück zum Zitat Linington C, Morgan BP, Scolding NJ et al (1989) The role of complement in the pathogenesis of experimental allergic encephalomyelitis. Brain 112:895–911PubMed Linington C, Morgan BP, Scolding NJ et al (1989) The role of complement in the pathogenesis of experimental allergic encephalomyelitis. Brain 112:895–911PubMed
57.
Zurück zum Zitat Vriesendorp FJ, Flynn RE, Pappolla MA, Koski CL (1997) Soluble complement receptor 1 (sCR59) is not as effective as cobra venom factor in the treatment of experimental allergic neuritis. Int J Neurosci 92:287–298PubMed Vriesendorp FJ, Flynn RE, Pappolla MA, Koski CL (1997) Soluble complement receptor 1 (sCR59) is not as effective as cobra venom factor in the treatment of experimental allergic neuritis. Int J Neurosci 92:287–298PubMed
63.
Zurück zum Zitat Hinson SR, McKeon A, Lennon VA (2010) Neurological autoimmunity targeting aquaporin-4. Neuroscience 168:1009–1018PubMed Hinson SR, McKeon A, Lennon VA (2010) Neurological autoimmunity targeting aquaporin-4. Neuroscience 168:1009–1018PubMed
64.
Zurück zum Zitat De Carvalho Jennings Pereira WL, Reiche EMV, Kallaur AP, Kaimen-Maciel DR (2015) Epidemiological, clinical, and immunological characteristics of neuromyelitis optica: a review. J Neurol Sci 355:7–17 De Carvalho Jennings Pereira WL, Reiche EMV, Kallaur AP, Kaimen-Maciel DR (2015) Epidemiological, clinical, and immunological characteristics of neuromyelitis optica: a review. J Neurol Sci 355:7–17
68.
Zurück zum Zitat Stanley KK, Herz J (1987) Topological mapping of complement component C9 by recombinant DNA techniques suggests a novel mechanism for its insertion into target membranes. EMBO J 6:1951–1957PubMedPubMedCentral Stanley KK, Herz J (1987) Topological mapping of complement component C9 by recombinant DNA techniques suggests a novel mechanism for its insertion into target membranes. EMBO J 6:1951–1957PubMedPubMedCentral
76.
Zurück zum Zitat Yang B, Brown D, Verkman AS (1996) The mercurial insensitive water channel (AQP-4) forms orthogonal arrays in stably transfected Chinese hamster ovary cells. J Biol Chem 271:4577–4580PubMed Yang B, Brown D, Verkman AS (1996) The mercurial insensitive water channel (AQP-4) forms orthogonal arrays in stably transfected Chinese hamster ovary cells. J Biol Chem 271:4577–4580PubMed
77.
Zurück zum Zitat Frigeri A, Gropper MA, Umenishi F et al (1995) Localization of MIWC and GLIP water channel homologs in neuromuscular, epithelial and glandular tissues. J Cell Sci 108(Pt 9):2993–3002PubMed Frigeri A, Gropper MA, Umenishi F et al (1995) Localization of MIWC and GLIP water channel homologs in neuromuscular, epithelial and glandular tissues. J Cell Sci 108(Pt 9):2993–3002PubMed
79.
Zurück zum Zitat Sabolić I, Herak-Kramberger CM, Breton S, Brown D (1999) Na/K-ATPase in intercalated cells along the rat nephron revealed by antigen retrieval. J Am Soc Nephrol 10:913–922PubMed Sabolić I, Herak-Kramberger CM, Breton S, Brown D (1999) Na/K-ATPase in intercalated cells along the rat nephron revealed by antigen retrieval. J Am Soc Nephrol 10:913–922PubMed
80.
Zurück zum Zitat Minami Y, Shimada S, Miyahara H et al (1998) Selective expression of mercurial-insensitive water channel (AQP-4) gene in Hensen and Claudius cells in the rat cochlea. Acta Otolaryngol Suppl 533:19–21PubMed Minami Y, Shimada S, Miyahara H et al (1998) Selective expression of mercurial-insensitive water channel (AQP-4) gene in Hensen and Claudius cells in the rat cochlea. Acta Otolaryngol Suppl 533:19–21PubMed
81.
Zurück zum Zitat Li J, Patil RV, Verkman AS (2002) Mildly abnormal retinal function in transgenic mice without Müller cell aquaporin-4 water channels. Invest Ophthalmol Vis Sci 43:573–579PubMed Li J, Patil RV, Verkman AS (2002) Mildly abnormal retinal function in transgenic mice without Müller cell aquaporin-4 water channels. Invest Ophthalmol Vis Sci 43:573–579PubMed
86.
103.
Zurück zum Zitat Kaplan M (2002) Eculizumab (Alexion). Curr Opin Investig Drugs 3:1017–1023PubMed Kaplan M (2002) Eculizumab (Alexion). Curr Opin Investig Drugs 3:1017–1023PubMed
110.
Zurück zum Zitat Patrick J, Lindstrom J (1973) Autoimmune response to acetylcholine receptor. Science 180:871–872PubMed Patrick J, Lindstrom J (1973) Autoimmune response to acetylcholine receptor. Science 180:871–872PubMed
112.
Zurück zum Zitat Newsom-Davis J, Pinching AJ, Vincent A, Wilson SG (1978) Function of circulating antibody to acetylcholine receptor in myasthenia gravis: investigation by plasma exchange. Neurology 28:266–272PubMed Newsom-Davis J, Pinching AJ, Vincent A, Wilson SG (1978) Function of circulating antibody to acetylcholine receptor in myasthenia gravis: investigation by plasma exchange. Neurology 28:266–272PubMed
113.
Zurück zum Zitat Lindstrom JM, Seybold ME, Lennon VA et al (1976) Antibody to acetylcholine receptor in myasthenia gravis. Prevalence, clinical correlates, and diagnostic value. Neurology 26:1054–1059PubMed Lindstrom JM, Seybold ME, Lennon VA et al (1976) Antibody to acetylcholine receptor in myasthenia gravis. Prevalence, clinical correlates, and diagnostic value. Neurology 26:1054–1059PubMed
114.
Zurück zum Zitat Lennon VA, Lambert EH (1980) Myasthenia gravis induced by monoclonal antibodies to acetylcholine receptors. Nature 285:238–240PubMed Lennon VA, Lambert EH (1980) Myasthenia gravis induced by monoclonal antibodies to acetylcholine receptors. Nature 285:238–240PubMed
115.
Zurück zum Zitat Rødgaard A, Nielsen FC, Djurup R et al (1987) Acetylcholine receptor antibody in myasthenia gravis: predominance of IgG subclasses 1 and 3. Clin Exp Immunol 67:82–88PubMedPubMedCentral Rødgaard A, Nielsen FC, Djurup R et al (1987) Acetylcholine receptor antibody in myasthenia gravis: predominance of IgG subclasses 1 and 3. Clin Exp Immunol 67:82–88PubMedPubMedCentral
116.
Zurück zum Zitat Heinemann S, Bevan S, Kullberg R et al (1977) Modulation of acetylcholine receptor by antibody against the receptor. Proc Natl Acad Sci USA 74:3090–3094PubMedPubMedCentral Heinemann S, Bevan S, Kullberg R et al (1977) Modulation of acetylcholine receptor by antibody against the receptor. Proc Natl Acad Sci USA 74:3090–3094PubMedPubMedCentral
120.
Zurück zum Zitat Almon RR, Andrew CG, Appel SH (1974) Serum globulin in myasthenia gravis: inhibition of alpha-bungarotoxin binding to acetylcholine receptors. Science 186:55–57PubMed Almon RR, Andrew CG, Appel SH (1974) Serum globulin in myasthenia gravis: inhibition of alpha-bungarotoxin binding to acetylcholine receptors. Science 186:55–57PubMed
121.
Zurück zum Zitat Gomez CM, Richman DP (1983) Anti-acetylcholine receptor antibodies directed against the alpha-bungarotoxin binding site induce a unique form of experimental myasthenia. Proc Natl Acad Sci USA 80:4089–4093PubMedPubMedCentral Gomez CM, Richman DP (1983) Anti-acetylcholine receptor antibodies directed against the alpha-bungarotoxin binding site induce a unique form of experimental myasthenia. Proc Natl Acad Sci USA 80:4089–4093PubMedPubMedCentral
122.
Zurück zum Zitat Hara H, Hayashi K, Ohta K et al (1993) Detection and characterization of blocking-type anti-acetylcholine receptor antibodies in sera from patients with myasthenia gravis. Clin Chem 39:2053–2057PubMed Hara H, Hayashi K, Ohta K et al (1993) Detection and characterization of blocking-type anti-acetylcholine receptor antibodies in sera from patients with myasthenia gravis. Clin Chem 39:2053–2057PubMed
123.
Zurück zum Zitat Lang B, Richardson G, Rees J et al (1988) Plasma from myasthenia gravis patients reduces acetylcholine receptor agonist-induced Na+ flux into TE671 cell line. J Neuroimmunol 19:141–148PubMed Lang B, Richardson G, Rees J et al (1988) Plasma from myasthenia gravis patients reduces acetylcholine receptor agonist-induced Na+ flux into TE671 cell line. J Neuroimmunol 19:141–148PubMed
131.
Zurück zum Zitat Williams CL, Hay JE, Huiatt TW, Lennon VA (1992) Paraneoplastic IgG striational autoantibodies produced by clonal thymic B cells and in serum of patients with myasthenia gravis and thymoma react with titin. Lab Invest 66:331–336PubMed Williams CL, Hay JE, Huiatt TW, Lennon VA (1992) Paraneoplastic IgG striational autoantibodies produced by clonal thymic B cells and in serum of patients with myasthenia gravis and thymoma react with titin. Lab Invest 66:331–336PubMed
134.
Zurück zum Zitat Skeie GO, Lunde PK, Sejersted OM et al (1998) Myasthenia gravis sera containing antiryanodine receptor antibodies inhibit binding of [3H]-ryanodine to sarcoplasmic reticulum. Muscle Nerve 21:329–335PubMed Skeie GO, Lunde PK, Sejersted OM et al (1998) Myasthenia gravis sera containing antiryanodine receptor antibodies inhibit binding of [3H]-ryanodine to sarcoplasmic reticulum. Muscle Nerve 21:329–335PubMed
135.
Zurück zum Zitat Romi F, Skeie GO, Vedeler C et al (2000) Complement activation by titin and ryanodine receptor autoantibodies in myasthenia gravis. A study of IgG subclasses and clinical correlations. J Neuroimmunol 111:169–176PubMed Romi F, Skeie GO, Vedeler C et al (2000) Complement activation by titin and ryanodine receptor autoantibodies in myasthenia gravis. A study of IgG subclasses and clinical correlations. J Neuroimmunol 111:169–176PubMed
142.
Zurück zum Zitat Lindstrom JM, Engel AG, Seybold ME et al (1976) Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies. J Exp Med 144:739–753PubMed Lindstrom JM, Engel AG, Seybold ME et al (1976) Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies. J Exp Med 144:739–753PubMed
143.
Zurück zum Zitat Nastuk WL, Plescia OJ, Osserman KE (1960) Changes in serum complement activity in patients with myasthenia gravis. Proc Soc Exp Biol Med 105:177–184PubMed Nastuk WL, Plescia OJ, Osserman KE (1960) Changes in serum complement activity in patients with myasthenia gravis. Proc Soc Exp Biol Med 105:177–184PubMed
145.
Zurück zum Zitat Sahashi K, Engel AG, Linstrom JM et al (1978) Ultrastructural localization of immune complexes (IgG and C3) at the end-plate in experimental autoimmune myasthenia gravis. J Neuropathol Exp Neurol 37:212–223PubMed Sahashi K, Engel AG, Linstrom JM et al (1978) Ultrastructural localization of immune complexes (IgG and C3) at the end-plate in experimental autoimmune myasthenia gravis. J Neuropathol Exp Neurol 37:212–223PubMed
146.
Zurück zum Zitat Fazekas A, Komoly S, Bozsik B, Szobor A (1986) Myasthenia gravis: demonstration of membrane attack complex in muscle end-plates. - PubMed - NCBI. Clin Neuropathol 2:78–83 Fazekas A, Komoly S, Bozsik B, Szobor A (1986) Myasthenia gravis: demonstration of membrane attack complex in muscle end-plates. - PubMed - NCBI. Clin Neuropathol 2:78–83
147.
Zurück zum Zitat Engel AG, Arahata K (1987) The membrane attack complex of complement at the endplate in myasthenia gravis. Ann N Y Acad Sci 505:326–332PubMed Engel AG, Arahata K (1987) The membrane attack complex of complement at the endplate in myasthenia gravis. Ann N Y Acad Sci 505:326–332PubMed
148.
Zurück zum Zitat Casali P, Borzini P, Zanussi C (1976) Letter: immune complexes in myasthenia gravis. Lancet (London, England) 2:378 Casali P, Borzini P, Zanussi C (1976) Letter: immune complexes in myasthenia gravis. Lancet (London, England) 2:378
149.
Zurück zum Zitat Barohn RJ, Brey RL (1993) Soluble terminal complement components in human myasthenia gravis. Clin Neurol Neurosurg 95:285–290PubMed Barohn RJ, Brey RL (1993) Soluble terminal complement components in human myasthenia gravis. Clin Neurol Neurosurg 95:285–290PubMed
150.
Zurück zum Zitat Kamolvarin N, Hemachudha T, Ongpipattanakul B et al (1991) Plasma C3c in immune-mediated neurological diseases: a preliminary report. Acta Neurol Scand 83:382–387PubMed Kamolvarin N, Hemachudha T, Ongpipattanakul B et al (1991) Plasma C3c in immune-mediated neurological diseases: a preliminary report. Acta Neurol Scand 83:382–387PubMed
151.
Zurück zum Zitat Basta M, Illa I, Dalakas MC (1996) Increased in vitro uptake of the complement C3b in the serum of patients with Guillain-Barré syndrome, myasthenia gravis and dermatomyositis. J Neuroimmunol 71:227–229PubMed Basta M, Illa I, Dalakas MC (1996) Increased in vitro uptake of the complement C3b in the serum of patients with Guillain-Barré syndrome, myasthenia gravis and dermatomyositis. J Neuroimmunol 71:227–229PubMed
153.
Zurück zum Zitat Lennon VA, Seybold ME, Lindstrom JM et al (1978) Role of complement in the pathogenesis of experimental autoimmune myasthenia gravis. J Exp Med 147:973–983PubMed Lennon VA, Seybold ME, Lindstrom JM et al (1978) Role of complement in the pathogenesis of experimental autoimmune myasthenia gravis. J Exp Med 147:973–983PubMed
154.
Zurück zum Zitat Christadoss P (1988) C5 gene influences the development of murine myasthenia gravis. J Immunol 140:2589–2592PubMed Christadoss P (1988) C5 gene influences the development of murine myasthenia gravis. J Immunol 140:2589–2592PubMed
155.
Zurück zum Zitat Tüzün E, Scott BG, Goluszko E et al (2003) Genetic evidence for involvement of classical complement pathway in induction of experimental autoimmune myasthenia gravis. J Immunol 171:3847–3854PubMed Tüzün E, Scott BG, Goluszko E et al (2003) Genetic evidence for involvement of classical complement pathway in induction of experimental autoimmune myasthenia gravis. J Immunol 171:3847–3854PubMed
156.
Zurück zum Zitat Biesecker G, Gomez CM (1989) Inhibition of acute passive transfer experimental autoimmune myasthenia gravis with Fab antibody to complement C6. J Immunol 142:2654–2659PubMed Biesecker G, Gomez CM (1989) Inhibition of acute passive transfer experimental autoimmune myasthenia gravis with Fab antibody to complement C6. J Immunol 142:2654–2659PubMed
161.
Zurück zum Zitat Asghar SS, Pasch MC (2000) Therapeutic inhibition of the complement system. Y2K update. Front Biosci 5:E63–E81PubMed Asghar SS, Pasch MC (2000) Therapeutic inhibition of the complement system. Y2K update. Front Biosci 5:E63–E81PubMed
163.
Zurück zum Zitat Piddlesden SJ, Jiang S, Levin JL et al (1996) Soluble complement receptor 1 (sCR166) protects against experimental autoimmune myasthenia gravis. J Neuroimmunol 71:173–177PubMed Piddlesden SJ, Jiang S, Levin JL et al (1996) Soluble complement receptor 1 (sCR166) protects against experimental autoimmune myasthenia gravis. J Neuroimmunol 71:173–177PubMed
169.
Zurück zum Zitat Zhou Y, Gong B, Lin F et al (2007) Anti-C5 antibody treatment ameliorates weakness in experimentally acquired myasthenia gravis. J Immunol 179:8562–8567PubMed Zhou Y, Gong B, Lin F et al (2007) Anti-C5 antibody treatment ameliorates weakness in experimentally acquired myasthenia gravis. J Immunol 179:8562–8567PubMed
173.
Zurück zum Zitat Dau PC (1982) Plasmapheresis in myasthenia gravis. Prog Clin Biol Res 88:265–285PubMed Dau PC (1982) Plasmapheresis in myasthenia gravis. Prog Clin Biol Res 88:265–285PubMed
177.
Zurück zum Zitat Palace J, Newsom-Davis J, Lecky B (1998) A randomized double-blind trial of prednisolone alone or with azathioprine in myasthenia gravis. Myasthenia Gravis Study Group. Neurology 50:1778–1783PubMed Palace J, Newsom-Davis J, Lecky B (1998) A randomized double-blind trial of prednisolone alone or with azathioprine in myasthenia gravis. Myasthenia Gravis Study Group. Neurology 50:1778–1783PubMed
Metadaten
Titel
Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review
verfasst von
Jayne L. Chamberlain
Saif Huda
Daniel H. Whittam
Marcelo Matiello
B. Paul Morgan
Anu Jacob
Publikationsdatum
03.09.2019
Verlag
Springer Berlin Heidelberg
Erschienen in
Journal of Neurology / Ausgabe 5/2021
Print ISSN: 0340-5354
Elektronische ISSN: 1432-1459
DOI
https://doi.org/10.1007/s00415-019-09498-4

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