| First Author | Wu GF | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 7 | Pages | 2064-73 |
| PubMed ID | 21469089 | Mgi Jnum | J:177316 |
| Mgi Id | MGI:5294730 | Doi | 10.1002/eji.201040809 |
| Citation | Wu GF, et al. (2011) Conditional deletion of SLP-76 in mature T cells abrogates peripheral immune responses. Eur J Immunol 41(7):2064-73 |
| abstractText | The adaptor protein Src homology 2 domain-containing leukocyte-specific protein of 76 kDa (SLP-76) is central to the organization of intracellular signaling downstream of the T-cell receptor (TCR). Evaluation of its role in mature, primary T cells has been hampered by developmental defects that occur in the absence of WT SLP-76 protein in thymocytes. Here, we show that following tamoxifen-regulated conditional deletion of SLP-76, mature, antigen-inexperienced T cells maintain normal TCR surface expression but fail to transduce TCR-generated signals. Conditionally deficient T cells fail to proliferate in response to antigenic stimulation or a lymphopenic environment. Mice with induced deletion of SLP-76 are resistant to induction of the CD4+ T-cell-mediated autoimmune disease experimental autoimmune encephalomyelitis. Altogether, our findings demonstrate the critical role of SLP-76-mediated signaling in initiating T-cell-directed immune responses both in vitro and in vivo and highlight the ability to analyze signaling processes in mature T cells in the absence of developmental defects. |
