Impaired T cell cross-talk in infection-associated immunopathology (P15)

我们假设感染相关的免疫病理学可能是由于免疫应答期间细胞通讯不足所致。我们将尝试通过调节效应T细胞上表达的特定受体-配体对的相互作用来干扰细胞串扰，然后监测对LCMV诱导的T细胞介导的免疫病理学发展的影响。具体而言，我们计划1）阐明活化T细胞表达CD 80的作用; 2）分析CXCL 10：CXCR 3和CCL 5：CCR 5在T细胞活化过程中的作用; 3）解决活化T细胞表达的可溶性共刺激/共抑制分子（如CD 80，CD 28，CTLA-4，PD-1，Lag 3和CD 160）是否有助于免疫病理学。

We hypothesize that infection-associated immunopathology can result from insufficient cellular communication during an immune response. We will attempt to interfere with cellular crosstalk by modulating the interaction of particular receptor-ligand pairs expressed on effector T cells, and then monitor the effect on the development of LCMV-induced T cell mediated immunopathology. Specifically, we plan to 1) elucidate the role of CD80 expression by activated T cells; 2) analyze the roles of CXCL10:CXCR3 and CCL5:CCR5 during T cell activation; and 3) address whether soluble co-stimulatory/co-inhibitory molecules expressed by activated T cells (such as CD80, CD28, CTLA-4, PD-1, Lag3 and CD160) contribute to immunopathology.