| First Author | Schneider H | Year | 2006 |
| Journal | Science | Volume | 313 |
| Issue | 5795 | Pages | 1972-5 |
| PubMed ID | 16931720 | Mgi Jnum | J:112894 |
| Mgi Id | MGI:3663963 | Doi | 10.1126/science.1131078 |
| Citation | Schneider H, et al. (2006) Reversal of the TCR stop signal by CTLA-4. Science 313(5795):1972-5 |
| abstractText | The coreceptor cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is pivotal in regulating the threshold of signals during T cell activation, although the underlying mechanism is still not fully understood. Using in vitro migration assays and in vivo two-photon laser scanning microscopy, we showed that CTLA-4 increases T cell motility and overrides the T cell receptor (TCR)-induced stop signal required for stable conjugate formation between T cells and antigen-presenting cells. This event led to reduced contact periods between T cells and antigen-presenting cells that in turn decreased cytokine production and proliferation. These results suggest a fundamentally different model of reverse stop signaling, by which CTLA-4 modulates the threshold for T cell activation and protects against autoimmunity. |
