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My project focuses on the contribution of the cell-surface receptor Tim-1 to helper CD4+ T cell function. Tim-1 is expressed by activated CD4+ T cells, dendritic cells, and B cells. Tim-1 polymorphisms in mice and humans have been implicated in allergic immune responses. Blocking antibodies to Tim-1 have been shown in mice to decrease airway hyperreactivity in a model of Th2 T cell-driven airway hyperreactivity. However, the role of Tim-1 as a general costimulatory molecule has also been postulated, and antibodies to Tim-1 have been shown to decrease disease in a mouse model of multiple sclerosis, a Th1/Th17-driven disease. Several groups have also demonstrated that Tim-1 may bind phosphatidylserine, a membrane lipid exposed on apoptotic cells. Impaired clearance of apoptotic cells is implicated in the development of autoimmune disease, further expanding the possible role that Tim-1 may play in immune system activation and regulation. Our goal is to characterize the role of Tim-1 in immune responses.
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