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. 2004 May 1;113(9):1328–1333. doi: 10.1172/JCI18838

Figure 2.

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.