| First Author | Zhong XP | Year | 2003 |
| Journal | Nat Immunol | Volume | 4 |
| Issue | 9 | Pages | 882-90 |
| PubMed ID | 12883552 | Mgi Jnum | J:85149 |
| Mgi Id | MGI:2672999 | Doi | 10.1038/ni958 |
| Citation | Zhong XP, et al. (2003) Enhanced T cell responses due to diacylglycerol kinase zeta deficiency. Nat Immunol 4(9):882-90 |
| abstractText | Much is known about how T cell receptor (TCR) engagement leads to T cell activation; however, the mechanisms terminating TCR signaling remain less clear. Diacylglycerol, generated after TCR ligation, is essential in T cells. Its function must be controlled tightly to maintain normal T cell homeostasis. Previous studies have shown that diacylglycerol kinase zeta (DGKzeta), which converts diacylglycerol to phosphatidic acid, can inhibit TCR signaling. Here we show that DGKzeta-deficient T cells are hyperresponsive to TCR stimulation both ex vivo and in vivo. Furthermore, DGKzeta-deficient mice mounted a more robust immune response to lymphocytic choriomeningitis virus infection than did wild-type mice. These results demonstrate the importance of DGKzeta as a physiological negative regulator of TCR signaling and T cell activation. |
