Herter, Jan M.Grabie, NirCullere, XavierAzcutia, VeronicaRosetti, FlorenciaBennett, PaulHerter-Sprie, Grit S.Elyaman, WassimLuscinskas, FrancisLichtman, AndrewMayadas, Tanya2016-02-012015Herter, J. M., N. Grabie, X. Cullere, V. Azcutia, F. Rosetti, P. Bennett, G. S. Herter-Sprie, et al. 2015. “AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation.” Nature Communications 6 (1): 10182. doi:10.1038/ncomms10182. http://dx.doi.org/10.1038/ncomms10182.2041-1723http://nrs.harvard.edu/urn-3:HUL.InstRepos:24983932The mechanisms driving T cell homing to lymph nodes and migration to tissue are well described but little is known about factors that affect T cell egress from tissues. Here, we generate mice with a T cell-specific deletion of the scaffold protein A kinase anchoring protein 9 (AKAP9) and use models of inflammatory disease to demonstrate that AKAP9 is dispensable for T cell priming and migration into tissues and lymph nodes, but is required for T cell retention in tissues. AKAP9 deficiency results in increased T cell egress to draining lymph nodes, which is associated with impaired T cell re-activation in tissues and protection from organ damage. AKAP9-deficient T cells exhibit reduced microtubule-dependent recycling of TCRs back to the cell surface and this affects antigen-dependent activation, primarily by non-classical antigen-presenting cells. Thus, AKAP9-dependent TCR trafficking drives efficient T cell re-activation and extends their retention at sites of inflammation with implications for disease pathogenesis.en-USJournal Article2016-02-0110.1038/ncomms10182