作者: Astrid Samuelsson , Terri L Towers , Jeffrey V Ravetch
DOI: 10.1126/SCIENCE.291.5503.484
关键词:
摘要: The molecular basis for the anti-inflammatory property of intravenous gamma globulin (IVIG) was investigated in a murine model immune thrombocytopenia. Administration clinically protective doses intact antibody or monomeric Fc fragments to wild-type Fcgamma receptor-humanized mice prevented platelet consumption triggered by pathogenic autoantibody. inhibitory receptor, FcgammaRIIB, required protection, because disruption either genetic deletion with blocking monoclonal reversed therapeutic effect IVIG. Protection associated ability IVIG administration induce surface expression FcgammaRIIB on splenic macrophages. Modulation signaling is thus potent strategy attenuating autoantibody-triggered inflammatory diseases.