Inhibition of Experimental Autoimmune Encephalomyelitis in Human C-Reactive Protein Transgenic Mice Is FcRIIB Dependent
Figure 2
CRP-mediated protection from EAE requires FcγRIIB. CRPtg versus littermate wildtype (a) or their respective counterparts lacking expression of FcγRI (b), FcγRIII (c), or FcγRIIB (d) were injected with MOG peptide, and EAE symptoms were monitored. Presence of the CRP transgene (closed circles in each panel) delayed onset of EAE in mice with intact FcγRs (a) and delayed onset and reduced severity of EAE in mice lacking FcγRI (b) or FcγRIII (c). In contrast in mice lacking FcγRIIB (d), expression of human CRP had no beneficial effect. See Table 1 for sample sizes and statistical analyses.
