| First Author | Ngiow SF | Year | 2011 |
| Journal | Cancer Res | Volume | 71 |
| Issue | 10 | Pages | 3540-51 |
| PubMed ID | 21430066 | Mgi Jnum | J:171999 |
| Mgi Id | MGI:5002754 | Doi | 10.1158/0008-5472.CAN-11-0096 |
| Citation | Ngiow SF, et al. (2011) Anti-TIM3 Antibody Promotes T Cell IFN-{gamma}-Mediated Antitumor Immunity and Suppresses Established Tumors. Cancer Res 71(10):3540-51 |
| abstractText | Strategies to activate and rescue exhausted tumor-specific T cells, including the use of monoclonal antibodies (mAb) that block the negative costimulatory receptors CTLA-4 and PD-1 are proving very effective, but TIM3 has been relatively neglected as a target. Here we report an extensive characterization of the therapeutic activity and mechanism of action of an anti-mouse TIM3 mAb against experimental and carcinogen-induced tumors. For the first time we specifically define the mechanism of antitumor action of anti-TIM3 requiring IFN-gamma producing CD8(+) T cells and CD4(+) T cells, and a higher ratio of tumor infiltrating CD8(+):CD4(+) T cells correlating with therapeutic success. Interestingly, in some models, anti-TIM3 appeared to be effective sometime before the appearance and accumulation of significant TIM3(+)PD-1(+) T cell populations in tumor bearing mice. Anti-TIM3 displayed modest prophylactic and therapeutic activity against a small fraction of carcinogen-induced sarcomas, but comparative and combination studies of anti-TIM3 with anti-CTLA-4 and anti-PD-1 against experimental and carcinogen-induced tumors suggested that these agents might be well-tolerated and very effective in combination. Cancer Res; 71(10); 3540-51. (c)2011 AACR. |
