期刊
BLOOD
卷 113, 期 5, 页码 1097-1104出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2008-05-158477
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资金
- Rudolf Virchow Center
- Program of Molecular Medicine at Hannover Medical School
- Deutsche Forschungsgemeinschaft [SFB 688, Ni556/7-1]
- German Excellence Initiative to the Graduate School of Life Sciences
- University of Wurzburg.
Fc gamma receptors (Fc gamma Rs) on mononuclear phagocytes trigger autoantibody and immune complex-induced diseases through coupling the self-reactive immunoglobulin G (IgG) response to innate effector pathways, such as phagocytosis, and the recruitment of inflammatory cells. FcR gamma-based activation is critical in the pathogenesis of these diseases, although the contribution of Fc gamma R-mediated calcium signaling in autoimmune injury is unclear. Here we show that macrophages lacking the endoplasmic reticulum resident calcium sensor, STIM1, cannot activate Fc gamma R-induced Ca2+ entry and phagocytosis. As a direct consequence, STIM1 deficiency results in resistance to experimental immune thrombocytopenia and anaphylaxis, autoimmune hemolytic anemia, and acute pneumonitis. These results establish STIM1 as a novel and essential component of Fc gamma R activation and also indicate that inhibition of STIM1-dependent signaling might become a new strategy to prevent or treat IgG-dependent immunologic diseases. (Blood. 2009;113:1097-1104)
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