Induction and suppression of collagen-induced arthritis is dependent on distinct fcgamma receptors.
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.
Kleinau
S
S
Department of Genetics and Pathology, Uppsala University, S-75185 Uppsala, Sweden. sandra.kleinau@genpat.uu.se
Martinsson
P
P
Heyman
B
B
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology*; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D007113:Immunity, Innate / Q000235:genetics; D051379:Mice; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains; D017452:Receptors, IgG / Q000172:deficiency / Q000235:genetics / Q000276:immunology*
D015703:Antigens, CD; D017452:Receptors, IgG