Programme(s) to which this project applies:
|☑ MPhil/PhD||☒ MRes[Med]||☒ URIS|
Sustained inflammation causes immune cell dysfunction and forms the common pathological basis for many chronic inflammatory diseases including autoimmunity, chronic viral infection and cancer. A key aspect of immune cell dysfunction that underpins the clinical outcome of these chronic conditions is the development of exhausted CD8+T cells. Increasing evidence suggests that CD8+T cell exhaustion is preceded by metabolic defects upon activation. However, the signals that drive this metabolic impairment remain largely undefined. Using murine models of chronic viral infections (lymphocytic choriomeningitis virus, LCMV), autoimmune disease (systemic lupus erythematous, SLE), and cancer (hepatocellular carcinoma, HCC) we aim to identify the key cytokine signals that impose metabolic stress in CD8+T cells and consequently dictate their fate decision towards exhaustion. The findings of this project will have a direct translational aspect where novel drug targets may be developed to restore T cell immunity in a broad inflammatory context.
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