| First Author | Ramsbottom KM | Year | 2014 |
| Journal | J Immunol | Volume | 192 |
| Issue | 2 | Pages | 553-7 |
| PubMed ID | 24337740 | Mgi Jnum | J:207326 |
| Mgi Id | MGI:5556009 | Doi | 10.4049/jimmunol.1302197 |
| Citation | Ramsbottom KM, et al. (2014) Cutting edge: DNAX accessory molecule 1-deficient CD8+ T cells display immunological synapse defects that impair antitumor immunity. J Immunol 192(2):553-7 |
| abstractText | DNAX accessory molecule 1 (DNAM-1) is expressed on all CD8(+) T cells and promotes their activation and effector function. DNAM-1 interacts with LFA-1, a critical molecule for immunological synapse formation between T cells and APCs, and for cytotoxic killing of target cells. Mice that lack DNAM-1 display abnormal T cell responses and antitumor activity; however, the mechanism involved is unclear. In this article, we show that DNAM-1 deficiency results in reduced proliferation of CD8(+) T cells after Ag presentation and impaired cytotoxic activity. We also demonstrate that DNAM-1-deficient T cells show reduced conjugations with tumor cells and decreased recruitment of both LFA-1 and lipid rafts to the immunological synapse, which correlates with reduced tumor cell killing in vitro. This synapse defect may explain why DNAM-1-deficient mice cannot clear tumors in vivo, and highlights the importance of DNAM-1 and the immunological synapse in T cell-mediated antitumor immunity. |
