Fc IgE receptors are found on immune effector cells and mediate macrophage phagocytosis, antibody-dependent cell-mediated cytotoxicity, mast cell degranulation, IgE-mediated systemic anaphylaxis and neutrophil recruitment.
These mice carry a targeted mutation of the Fcer1g (Fc receptor, IgE, high affinity I, gamma polypeptide ) gene and have been backcrossed onto the autoimmune-susceptible DBA/1 background. In homozygous mice challenged with collagen-induced arthritis, fewer mice develop arthritic symptoms, and the symptoms are mild compared to wildtype controls. Mutant mice that develop collagen-induced arthritis do not exhibit inflammatory cell infiltration in the synovium or cartilage and bone erosion. However, homozygotes produce total IgG anti-collagen antibodies at levels similar to those seen in controls. During backcrossing, the Y chromosome may not have been fixed to the DBA/1 genetic background. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size.
