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).
Full Text
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call