Figure 3.

C5-mediated arthritis in K/BxN mice occurs in the absence of C3 and FcRγ. (a) Null alleles of C3 and Fcer1g (encoding FcRγ) were bred into the K/BxN mouse system. The development of arthritis was assessed in C3/FcRγ-deficient K/BxN mice bearing homozygous null alleles at both loci (open squares, n = 4) and in littermate controls expressing one wild-type allele at each locus (filled squares, n = 4). Data are mean ± standard error of the mean (SEM); there are no statistical differences at any of the time points for these two groups. Treatment of the C3/FcRγ-deficient K/BxN mice with anti-C5 antibody reduced arthritis severity (filled diamonds, n = 3); *P < 0.05 for the anti-C5 antibody-treated C3/FcRγ-deficient mice compared with untreated C3/FcRγ-deficient mice. (b) A naturally occurring null allele of Hc (encoding C5) and the targeted null allele of Fcer1g were bred into K/BxN mice. The development of arthritis was assessed in C5/FcRγ-deficient K/BxN mice (open triangles, n = 8) and in littermate controls with one wild-type allele at each locus (filled triangles, n = 8). Data are mean ± SEM; **P < 0.01; ***P < 0.001. FcRγ, the cytoplasmic signaling chain shared by activating Fc receptors for immunoglobulin G; NS, not significant.

Auger et al. Arthritis Research & Therapy 2012 14:R269   doi:10.1186/ar4117
Download authors' original image