| First Author | Braun A | Year | 2009 |
| Journal | Blood | Volume | 113 |
| Issue | 5 | Pages | 1097-104 |
| PubMed ID | 18941110 | Mgi Jnum | J:144644 |
| Mgi Id | MGI:3831463 | Doi | 10.1182/blood-2008-05-158477 |
| Citation | Braun A, et al. (2009) STIM1 is essential for Fcgamma receptor activation and autoimmune inflammation. Blood 113(5):1097-104 |
| abstractText | Fcgamma receptors (FcgammaRs) 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. FcRgamma-based activation is critical in the pathogenesis of these diseases, although the contribution of FcgammaR-mediated calcium signaling in autoimmune injury is unclear. Here we show that macrophages lacking the endoplasmic reticulum-resident calcium sensor, STIM1, cannot activate FcgammaR-induced Ca(2+) 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 FcgammaR activation and also indicate that inhibition of STIM1-dependent signaling might become a new strategy to prevent or treat IgG-dependent immunologic diseases. |
