Abstract
Systemic sclerosis (SSc) is a systemic autoimmune disease characterized by excessive fibrosis of the skin and internal organ. FcγRIIB, a low-affinity receptor for the Fc fragment of IgG, is expressed on the surface of several leukocyte subsets and functions in negative feedback pathways to down-regulate B cell antigen receptor signaling. To elucidate the role of FcγRIIB in the development of fibrosis, a murine bleomycin (BLM)-induced scleroderma model was examined in mice lacking FcγRIIB (FcγRIIB-/- mice).
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