NIH Research Festival
T cell trafficking between the blood and lymphoid organs is essential for the function of the adaptive immune system. Lymphocyte homing to lymph nodes requires that they cross endothelial barriers present in blood vessels and lymphatics. This multi-step process requires a remodeling of the lymphocyte plasma membrane, which is mediated by the constant re-arrangement of the actin cytoskeleton. Pak1 plays a central role in cell morphology, adhesion and migration in various cell types. Here we demonstrate that Pak1 is required for activated CD4+ T cell trafficking to lymph nodes. Pak1 deficiency causes a defect in the transcription of CCR7 and CD62L, thereby altering lymphocyte trafficking. Additionally, we found an increase in CD62L shedding in Pak1-deficient T cells, which was enhanced by a decrease in the recruitment of calmodulin to the cytoplasmic tail of CD62L with T cell activation. Overall, our findings demonstrate that by regulating the expression of two major lymph node-homing molecules, CD62L and CCR7, Pak1 mediates activated CD4+ T cell trafficking.
Scientific Focus Area: Immunology
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