| First Author | Li J | Year | 2008 |
| Journal | J Neuroimmunol | Volume | 194 |
| Issue | 1-2 | Pages | 44-53 |
| PubMed ID | 18207575 | Mgi Jnum | J:131899 |
| Mgi Id | MGI:3774797 | Doi | 10.1016/j.jneuroim.2007.11.005 |
| Citation | Li J, et al. (2008) Inhibitory IgG receptor FcgammaRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis. J Neuroimmunol 194(1-2):44-53 |
| abstractText | Deficiency of the inhibitory FcgammaRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcgammaRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcgammaRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcgammaRIIB 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 FcgammaRIIB promotes antibody-mediated autoimmunity. |
