T cell immunoglobulin and mucin-domain-containing molecule 3 (Tim-3), which could be identified as a specific cell surface marker of T-helper 1 (Th1) CD4+ T cells, is one of the Ig superfamily members and is preferentially expressed on fully differentiated Th1 lymphocytes but not on Th2 cells. Studies have shown that TIM-3 / HAVCR2 may not contribute to the T cell differentiation but might perform a critical function in the Th1 cell transportation. Galectin-9 & TIM-3 immune checkpoint pathway inhibits Th1 and Th17 responses and induces peripheral tolerance, suggesting an inhibitory role of TIM-3 / HAVCR2 in T cell responses. The soluble form of TIM-3 / HAVCR2 would reduce the antigen-specific T cell responses and downregulate the anti-tumor immunity in vivo by inhibiting the Th1 responses.
Galectin-9 & TIM-3 immune checkpoint pathway immunemediats the tumor microenvironment inhibition by different mechanisms, and plays an important role in tumorigenesis, development, invasion and metastasis. Several studies have found that TIM-3 / HAVCR2 is highly expressed on the tumor infiltrating T cells of the solid tumor, and the high expression of TIM-3 / HAVCR2 is related with the tumorigenesis and tumor development. Our team previously showed that TIM-3 / HAVCR2 expression characterized regulatory T cells in lung cancer tissues and was associated with tumor progression. However, the related research of the expression and role of the TIM-3 / HAVCR2 in non-solid tumors, such as acute myeloid leukemia (AML) is rare.
Ying Ju et al. T cell immunoglobulin- and mucin-domain-containing molecule-3 (Tim-3) mediates natural killer cell suppression in chronic hepatitis B.J Hepatol. 2010 Mar;52(3):322-9.