| First Author | Kleinau S | Year | 2000 |
| Journal | J Exp Med | Volume | 191 |
| Issue | 9 | Pages | 1611-6 |
| PubMed ID | 10790435 | Mgi Jnum | J:61920 |
| Mgi Id | MGI:1855770 | Doi | 10.1084/jem.191.9.1611 |
| Citation | Kleinau S, et al. (2000) Induction and suppression of collagen-induced arthritis is dependent on distinct fcgamma receptors. J Exp Med 191(9):1611-6 |
| abstractText | Receptors for immunoglobulin (Ig)G (FcgammaRs) are important for the antibody-mediated effector functions of the immune system. FcgammaRI and FcgammaRIII trigger cell activation through a common gamma chain, whereas FcgammaRII acts as a negative regulator of antibody production and immune complex-triggered activation. Here we describe the in vivo consequences of FcgammaR deficiency in a mouse model of human rheumatoid arthritis. FcRgamma chain-deficient mice on arthritis-susceptible DBA/1 background were immunized with collagen for induction of collagen-induced arthritis. The DBA/1 mice lacking FcRgamma chain were protected from collagen-induced arthritis in contrast to wild-type mice, although both groups produced similar levels of IgG anticollagen antibodies. In comparison, DBA/1 mice lacking FcgammaRII developed an augmented IgG anticollagen response and arthritis. These observations suggest a crucial role of FcgammaRI and FcgammaRIII in triggering autoimmune arthritis. |
