The MHC class I–like Fc receptor promotes humorally mediated autoimmune disease
J. Clin. Invest. Shreeram Akilesh, et al. 113:1328 doi:10.1172/JCI18838 [Go to this article.]

Figure 2
FcRn-deficient K/BxN mice are protected from genetically-induced arthritis. (A) Ankle width measurements and overall arthritis scores (mean ± SE) were performed as in Figure 1. All WT FcRn^+/_ littermates (filled diamonds; n = 21; 13 males and 8 females) showed rapid disease onset. Of 21 FcRn^_/_ littermates, the mice that remained healthy (open circles; n = 10; 4 males and 6 females) at approximately the 16-week duration of the experiment are plotted separately from FcRn^_/_ mice (n = 11; 3 males and 8 females) that became sick (filled circles). The time of disease onset of healthy mice versus WT FcRn^+/_ littermates versus FcRn^_/_ sick mice was significant at P < 0.0001 by the ANOVA repeated measures test. (B) H&E sections of representative 16-week K/BxN-FcRn^+/_ (+/_), sick FcRn^_/_ (_/_ sick), and healthy FcRn^_/_ (_/_ healthy) mice at ∞20 magnification. (C) Total serum IgG and (D) anti-GPI activity of each cohort from A was measured by ELISA at the weekly time points indicated. IgG levels of FcRn^_/_ healthy versus WT FcRn^+/_ mice and FcRn^_/_ sick versus WT FcRn^+/_ mice was significant at P _ 0.0001 by the Scheffe test. FcRn^_/_ healthy versus FcRn^_/_ sick (filled circles) mice did not differ significantly by the Scheffe test. Anti-GPI levels of FcRn^_/_ healthy mice versus WT FcRn^+/_ mice versus FcRn^_/_ sick mice was significant at P _ 0.0004 by the Scheffe test. conc, concentration.