| First Author | Beyersdorf N | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 6 | Pages | 3390-7 |
| PubMed ID | 19265116 | Mgi Jnum | J:145932 |
| Mgi Id | MGI:3836340 | Doi | 10.4049/jimmunol.0802888 |
| Citation | Beyersdorf N, et al. (2009) STIM1-independent T cell development and effector function in vivo. J Immunol 182(6):3390-7 |
| abstractText | Store-operated Ca(2+) entry (SOCE) is believed to be of pivotal importance in T cell physiology. To test this hypothesis, we generated mice constitutively lacking the SOCE-regulating Ca(2+) sensor stromal interaction molecule 1 (STIM1). In vitro analyses showed that SOCE and Ag receptor complex-triggered Ca(2+) flux into STIM1-deficient T cells is virtually abolished. In vivo, STIM1-deficient mice developed a lymphoproliferative disease despite normal thymic T cell maturation and normal frequencies of CD4(+)Foxp3(+) regulatory T cells. Unexpectedly, STIM1-deficient bone marrow chimeric mice mounted humoral immune responses after vaccination and STIM1-deficient T cells were capable of inducing acute graft-versus-host disease following adoptive transfer into allogeneic hosts. These results demonstrate that STIM1-dependent SOCE is crucial for homeostatic T cell proliferation, but of much lesser importance for thymic T cell differentiation or T cell effector functions. |
