10.3389/fimmu.2019.00370.s004 Ana Dios-Esponera Ana Dios-Esponera Nicolas Melis Nicolas Melis Bhagawat C. Subramanian Bhagawat C. Subramanian Roberto Weigert Roberto Weigert Lawrence E. Samelson Lawrence E. Samelson Video_3_Pak1 Kinase Promotes Activated T Cell Trafficking by Regulating the Expression of L-Selectin and CCR7.AVI Frontiers 2019 Pak1 kinase L-selectin CCR7 lymph node trafficking L-selectin shedding 2019-03-05 04:08:49 Media https://frontiersin.figshare.com/articles/media/Video_3_Pak1_Kinase_Promotes_Activated_T_Cell_Trafficking_by_Regulating_the_Expression_of_L-Selectin_and_CCR7_AVI/7801379 <p>Normal function of the adaptive immune system requires trafficking of T cells between the blood and lymphoid organs. 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 dynamic 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<sup>+</sup> T cell trafficking to lymph nodes. Pak1 deficiency in T cells causes a defect in the transcription of CCR7 and L-selectin, thereby altering lymphocyte trafficking. Additionally, we report an increase in L-selectin shedding in Pak1-deficient T cells, which correlates with a decrease in the recruitment of calmodulin to the cytoplasmic tail of L-selectin during T cell activation. Overall, our findings demonstrate that by regulating the expression of two major lymph node homing molecules, L-selectin and CCR7, Pak1 mediates activated CD4<sup>+</sup> T cell trafficking.</p>