Abstract

Abstract There is a progressive TIM-3+ T reg increase in solid tumors as the tumor progress. W have found that knocking out the ability of T reg to induce TIM-3 lead to delayed progression of tumors in the TIM-3 conditional knockout mice upon both hot (MC38) and cold (B16F10) syngeneic tumor challenges. We are employing our conditional T reg specific TIM-3 Knockout mouse to study if presence or absence of TIM-3 on T reg cells within these tumor models. Preliminary data has shown that our conditional Tim3 knockout T reg cells are found at a much lower frequency, and have an altered suppressive phenotype within the microenvironment of these tumors. We are currently investigating the other changes in the different subsets of lymphoid compartment in tumors. These data suggest that altering the expression of TIM-3+ on T reg has the potential to act as an effective target to alter tumor microenvironment. Targeting TIM-3+ T reg may therefore be attractive model to study, along with other combination immunotherapy to increase the success in immunotherapy on patients who develop resistance to primary immunotherapy.

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