TIM3 or T-cell Immunoglobulin domain and Mucin domain 3 can be expressed on both tumor and immune cells including T helper type 1 (Th1) cells, Th17 and CD8+ T cells, tumor infiltrating lymphocytes (TILs), regulatory T cells and innate immune cells (1). TIM3 acts as a negative regulator of Th1/Tc1 (T cytotoxic type 1) function by triggering cell death upon interaction with its ligand, galectin-9 (2,3). Co-blockade of TIM3 and programmed cell death 1 (PD1) can result in tumor regression in preclinical models of melanoma, colorectal cancer, and acute myeloid leukemia (AML). In patients with more advanced cancers, co-blockade of TIM3 and PD1 can improve anticancer T cell response (4). An increasing number of preclinical studies have reported that TIM3 may improve immunotherapy outcomes in various cancers including melanoma, ovarian cancer, colon cancer, AML, and gastric cancer (5).
1. Friedlaender A, et al. New emerging targets in cancer immunotherapy: the role of TIM3. ESMO Open. 2019;4(Suppl 3): e000497.
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3. Syn, et al. De-novo and acquired resistance to immune checkpoint targeting. The Lancet Oncology 2017; 18 (12): e731–e41.
4. Wolf Y, et al. TIM3 comes of age as an inhibitory receptor. Nat Rev Immunol. 2020;20(3):173-85.
5. He Y, et al. TIM-3, a promising target for cancer immunotherapy. Onco Targets Ther. 2018; 11:7005-09.
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