Complement associated pathogenic mechanisms in myasthenia gravis.

Abstract:

:The complement system is profoundly involved in the pathogenesis of acetylcholine receptor (AChR) antibody (Ab) related myasthenia gravis (MG) and its animal model experimental autoimmune myasthenia gravis (EAMG). The most characteristic finding of muscle pathology in both MG and EAMG is the abundance of IgG and complement deposits at the nerve-muscle junction (NMJ), suggesting that AChR-Ab induces muscle weakness by complement pathway activation and consequent membrane attack complex (MAC) formation. This assumption has been supported with EAMG resistance of complement factor C3 knockout (KO), C4 KO and C5 deficient mice and amelioration of EAMG symptoms following treatment with complement inhibitors such as cobra venom factor, soluble complement receptor 1, anti-C1q, anti-C5 and anti-C6 Abs. Moreover, the complement inhibitor decay accelerating factor (DAF) KO mice exhibit increased susceptibility to EAMG. These findings have brought forward improvisation of novel therapy methods based on inhibition of classical and common complement pathways in MG treatment.

journal_name

Autoimmun Rev

journal_title

Autoimmunity reviews

authors

Tüzün E,Christadoss P

doi

10.1016/j.autrev.2013.03.003

subject

Has Abstract

pub_date

2013-07-01 00:00:00

pages

904-11

issue

9

eissn

1568-9972

issn

1873-0183

pii

S1568-9972(13)00029-3

journal_volume

12

pub_type

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