The Fc low affinity IgE receptor is found on B cells, follicular dendritic cells, and a subset of T cells mediating IgE synthesis and regulation, IgE-dependent cytotoxicity, and B-cell activation and growth. These mice carry a targeted mutation of the Fcer2a (Fc receptor, IgE, low affinity II, alpha polypeptide) gene and have been backcrossed onto the autoimmune-susceptible DBA/1 background. Homozygotes are resistant to collagen-induced arthritis, with the few affected mutants developing mild arthritis. Time to onset of symptoms is delayed compared to controls. Four weeks after the collagen challenge up to 17% of the homozygous mice develop symptoms compared with 50-64% of the wildtype controls. However, incidence of disease in both mutant and wildtype mice is similar after 10 weeks. Both Anti-Collagen IgG antibodies and TNFalpha levels found in homozygous mice are similar to levels seen in controls. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. During backcrossing, the Y chromosome may not have been fixed to the DBA/1 genetic background.
