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In this talk I will discuss how inflammation and end-stage (senescent) T cells collaborate to induce immunopathology in the skin, using human cutaneous leishmaniasis as a model. The interactions involved are likely to translate to many other clinical situatioins where senescent T cells and infammatioin co-exist in tissue envirionments. This raises the question of how best to tackle the problem and to reduce tissue damage. Should the T cells themselves, or the inflamed microenviroenviromnent, or both be the focus of drug targets.
