Cytokine-induced modulation of T cell antigen receptor signaling

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Killer T lymphocytes are important mediators of autoimmune diseases, but they must be activated before they can induce tissue damage. In most cases of autoimmune diseases, it remains unknown what triggers the ability of potentially self-reactive T cells to damage healthy tissues. Current evidence suggests that appropriate genetic and environmental factors must interact in certain ways to stimulate potentially self-destructive killer T cells. One of these environmental factors is thought to be microbial pathogens. Certain viruses and bacteria are believed to be associated with the initiation, progression and exacerbation of autoimmune diseases. However, pathogens implicated in one single autoimmune disease may be very diverse and have nothing in common. This implies that pathogens per se may not directly induce autoimmune diseases. Therefore, we speculate that certain factors that are similarly affected by different pathogens might underlie various pathogen-associated autoimmune diseases. We have observed that one group of inflammatory factors induced by microbes, called cytokines, can activate killer T cells in an unconventional manner and increase their reactivity to body's own tissues. In this project, we investigate how cytokines aberrantly boost the ability of killer T cells to recognize and kill healthy tissues leading to autoimmune diseases.