| First Author | Zhu M | Year | 2006 |
| Journal | Immunity | Volume | 25 |
| Issue | 5 | Pages | 757-68 |
| PubMed ID | 17081783 | Mgi Jnum | J:116157 |
| Mgi Id | MGI:3693063 | Doi | 10.1016/j.immuni.2006.08.025 |
| Citation | Zhu M, et al. (2006) Negative regulation of T cell activation and autoimmunity by the transmembrane adaptor protein LAB. Immunity 25(5):757-68 |
| abstractText | LAB (linker for activation of B cells), also known as NTAL (non-T cell activation linker), is a LAT (linker for activation of T cells)-like adaptor protein that is expressed in B, NK, and mast cells. Its role in lymphocytes has not been clearly demonstrated. Here, we showed that aged LAB-deficient (Lat2(-/-)) mice developed an autoimmune syndrome. Lat2(-/-) T cells were hyperactivated and produced more cytokines than Lat2(+/+) T cells. Even though LAB was absent in naive T cells, LAB could be detected in activated Lat2(+/+) T cells. LAT-mediated signaling events were enhanced in Lat2(-/-) T cells; however, they were suppressed in T cells that overexpressed LAB. Mice with the Lat2 gene conditionally deleted from T cells also developed the autoimmune syndrome like Lat2(-/-) mice. Together, these data demonstrated an important role of LAB in limiting autoimmune response and exposed a mechanism regulating T cell activation. |
