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dc.contributor.authorHerter, Jan M.en_US
dc.contributor.authorGrabie, Niren_US
dc.contributor.authorCullere, Xavieren_US
dc.contributor.authorAzcutia, Veronicaen_US
dc.contributor.authorRosetti, Florenciaen_US
dc.contributor.authorBennett, Paulen_US
dc.contributor.authorHerter-Sprie, Grit S.en_US
dc.contributor.authorElyaman, Wassimen_US
dc.contributor.authorLuscinskas, Francis W.en_US
dc.contributor.authorLichtman, Andrew H.en_US
dc.contributor.authorMayadas, Tanya N.en_US
dc.date.accessioned2016-02-01T15:45:40Z
dc.date.issued2015en_US
dc.identifier.citationHerter, 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.en
dc.identifier.issn2041-1723en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:24983932
dc.description.abstractThe 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
dc.language.isoen_USen
dc.publisherNature Publishing Groupen
dc.relation.isversionofdoi:10.1038/ncomms10182en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4703868/pdf/en
dash.licenseLAAen_US
dc.titleAKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammationen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature Communicationsen
dash.depositing.authorHerter, Jan M.en_US
dc.date.available2016-02-01T15:45:40Z
dc.identifier.doi10.1038/ncomms10182*
dash.authorsorderedfalse
dash.contributor.affiliatedGrabie, Nir
dash.contributor.affiliatedHerter-Sprie, Grit S.
dash.contributor.affiliatedMayadas, Tanya
dash.contributor.affiliatedElyaman, Wassim
dash.contributor.affiliatedHerter, Jan M.
dash.contributor.affiliatedLuscinskas, Francis
dash.contributor.affiliatedLichtman, Andrew


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