Elucidating the effects of insulin signalling on T cell metabolism and effector function within the tumour microenvironment

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Recent evidence has shown the importance of insulin signalling for activated T cells, supporting metabolic reprogramming and enhancing effector function in viral infection and autoimmunity models. Our group has identified that insulin levels are profoundly diminished within interstitial fluid extracted from tumours, suggesting that abrogated insulin signalling could partially explain metabolic insufficiencies of effector T cells within tumours. My project will test the hypothesis that insulin availability in the tumour microenvironment is limited, restricting glucose uptake, T cell activation and ultimately hampering effective anti-tumour immunity and immunotherapy. We will test the hypothesis using murine tumour models, CRISPR-mediated knockout systems, in vitro functional assays, epigenomic and transcriptomic techniques