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• W2114238926 abstract "Abstract 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-γ 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. ©2011 AACR." @default.
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• W2114238926 date "2011-05-15" @default.
• W2114238926 modified "2023-10-17" @default.
• W2114238926 title "Anti-TIM3 Antibody Promotes T Cell IFN-γ–Mediated Antitumor Immunity and Suppresses Established Tumors" @default.
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• W2114238926 doi "https://doi.org/10.1158/0008-5472.can-11-0096" @default.
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• W2114238926 hasPublicationYear "2011" @default.
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