Abstract
The role of regulators of complement activity (RCA) involving CD55 and CD59 in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG) remains unclear. CD55 and CD59 restrict complement activation by inhibiting C3/C5 convertases' activities and membrane attack complex formation, respectively. Actively immunized EAMG mice deficient in either CD55 or CD59 showed significant differences in adaptive immune responses and worsened disease outcome associated with increased levels of serum cytokines, modified production of acetylcholine receptor antibodies, and more complement deposition at the neuromuscular junction. We conclude that modulation of complement activity by RCA represents an alternative in controlling of autoimmune processes in EAMG.
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