| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3065347 | Journal of Neuroimmunology | 2008 | 10 Pages |
Abstract
Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4+CD25+ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.
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Authors
Jing Li, Erdem Tüzün, Xiong Rong Wu, Hui Bin Qi, Windy Allman, Shamsher S. Saini, Premkumar Christadoss,