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 1
FcRn-deficient mice are resistant to serum-transfer arthritis. Data represented as the mean ± SE. (A_C) A single injection of 250 ∝l of sera pooled from 6- to 20-week-old arthritic K/BxN animals was injected intraperitoneally into three FcRn^_/_ (open circles) and three FcRn^+/+ (filled circles) B6 control mice. (A) Ankle width determinations and overall arthritis scores are as described (19). All time points except day 0 were significant at P < 0.05. (B) Digital images of representative ankles of FcRn^_/_ and WT mice 6 days after serum transfer. (C) Serial serum samples from A were analyzed for anti-GPI Ig by ELISA (21). Data are representative of two independent experiments. NS, not significant. All other time points were significant at P < 0.05. (D) Ankle width and arthritis scores of B6-FcRn^_/_ mice (n = 4_5) injected intraperitoneally with 250 (filled circles), 500 (filled squares), or 1,000 (open squares) ∝l arthritogenic K/BxN or 1,000 ∝l normal B6 mouse serum (open circles). *Ankle width and arthritis score time points were P _ 0.004 and P < 0.01 versus B6 serum, respectively. Other time points versus B6 serum were not significant at P < 0.05.