| First Author | Shen S | Year | 2010 |
| Journal | J Biol Chem | Volume | 285 |
| Issue | 46 | Pages | 35393-405 |
| PubMed ID | 20837489 | Mgi Jnum | J:166860 |
| Mgi Id | MGI:4849896 | Doi | 10.1074/jbc.M110.145052 |
| Citation | Shen S, et al. (2010) The importance of LAT in the activation, homeostasis, and regulatory function of T cells. J Biol Chem 285(46):35393-405 |
| abstractText | LAT (linker for activation of T cells) is a transmembrane adaptor protein that plays an essential role in TCR-mediated signaling and thymocyte development. Because LAT-deficient mice have an early block in thymocyte development, we utilized an inducible system to delete LAT in primary T cells to study LAT function in T cell activation, homeostasis, and survival. Deletion of LAT caused primary T cells to become unresponsive to stimulation from the TCR and impaired T cell homeostatic proliferation and long term survival. Furthermore, deletion of LAT led to reduced expression of Foxp3, CTLA-4, and CD25 in T(reg) cells and impaired their function. Consequently, mice with LAT deleted developed a lymphoproliferative syndrome similar to that in LATY136F mice, although less severe. Our data implicate that LAT has positive and negative roles in the regulation of mature T cells. |
