| First Author | Herter JM | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 10182 | PubMed ID | 26680259 |
| Mgi Jnum | J:228425 | Mgi Id | MGI:5707083 |
| Doi | 10.1038/ncomms10182 | Citation | Herter JM, et al. (2015) AKAP9 regulates activation-induced retention of T lymphocytes at sites of inflammation. Nat Commun 6:10182 |
| abstractText | 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. |
