AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation

Jan M. Herter, Nir Grabie, Xavier Cullere, Veronica Azcutia, Florencia Rosetti, Paul Bennett, Grit S. Herter-Sprie, Wassim Elyaman, Francis W. Luscinskas, Andrew H. Lichtman and Tanya N. Mayadas ()
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Jan M. Herter: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Nir Grabie: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Xavier Cullere: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Veronica Azcutia: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Florencia Rosetti: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Paul Bennett: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Grit S. Herter-Sprie: Dana-Farber Cancer Institute and Harvard Medical School
Wassim Elyaman: Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital and Harvard Medical School
Francis W. Luscinskas: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Andrew H. Lichtman: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur
Tanya N. Mayadas: Center for Excellence in Vascular Biology, Brigham and Women’s Hospital and Harvard Medical School, 77 Avenue Louis Pasteur

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract The 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.

Date: 2015
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DOI: 10.1038/ncomms10182

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