Figure 6: The pathogenesis of IC-mediated bone loss.

(a) IgG IC-induced bone loss in the calvarial bone of WT, Fcgr2b^−/−, Fcgr3^−/− and Fcer1g^−/− mice. Representative data of nine mice are shown. (b) Effect of IgG1 IC on systemic bone loss in Fcgr2b^+/− and Fcgr2b^−/− mice. Representative data of 10 mice are shown. (c) The serum level of tumour necrosis factor (TNF)-α and interleukin (IL)-1β in Fcgr2b^+/− and Fcgr2b^−/− mice injected with the IgG1 ICs. Twenty-week-old Fcgr2b^−/− mice were analysed as control mice for serum cytokine production (n=10). (d) Effect of serum IgG derived from a CIA model mouse on the osteoclastogenesis of BMMs from control or CIA mice. (e) PLCγ2 phosphorylation and NFATc1 induction of cells derived from a CIA mouse during RANKL-induced osteoclastogenesis in the presence of CIA serum. (f) The effect of mRNA expression of FcγR, FcγRIIB, FcγRIII and FcγRV on bone marrow cells derived from control and CIA mice. (g) Effect of IgG ICs on the osteoclastogenesis of BMMs from control and CIA mice. (h) Effect of retrovirus-mediated knockdown of FcγRIII expression on IgG1 IC-mediated osteoclastogenesis in BMMs derived from CIA mice. (i) Effect of knockdown of FcγRIV expression on IgG2a IC-mediated osteoclastogenesis in BMMs derived from CIA mice. All quantification experiments were performed using culture wells or samples. All data are representative of more than six independent experiments and are shown as the mean±s.e.m. Statistical analyses were performed using unpaired two-tailed Student’s t-test (*P<0.05; **P<0.01; n.s., not significant).