Genetic evidence for the involvement of Fcgamma receptor III in experimental autoimmune myasthenia gravis pathogenesis

Journal of Neuroimmunology
Erdem TüzünPremkumar Christadoss

Abstract

Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcgammaRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcgamma receptor involvement in EAMG pathogenesis.

References

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Citations

May 6, 2008·Journal of Neuroimmunology·Huibin QiPremkumar Christadoss
Jun 24, 2008·Annals of the New York Academy of Sciences·Premkumar ChristadossHuan Yang
Jun 24, 2008·Annals of the New York Academy of Sciences·Matthieu GiraudHenri-Jean Garchon
Jan 1, 2008·Expert Review of Clinical Immunology·Linda L KusnerJindrich Soltys
Apr 16, 2014·Reviews in the Neurosciences·Ruksana HudaPremkumar Christadoss
Aug 28, 2012·Journal of Clinical Neuromuscular Disease·Carolina BarnettVera Bril

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