| First Author | Hwang IY | Year | 2017 |
| Journal | J Immunol | Volume | 198 |
| Issue | 7 | Pages | 2721-2734 |
| PubMed ID | 28235863 | Mgi Jnum | J:247663 |
| Mgi Id | MGI:5926430 | Doi | 10.4049/jimmunol.1601433 |
| Citation | Hwang IY, et al. (2017) Normal Thymocyte Egress, T Cell Trafficking, and CD4+ T Cell Homeostasis Require Interactions between RGS Proteins and Galphai2. J Immunol 198(7):2721-2734 |
| abstractText | Adaptive immunity depends on mature thymocytes leaving the thymus to enter the bloodstream and the trafficking of T cells through lymphoid organs. Both of these require heterotrimeric Galphai protein signaling, whose intensity and duration are controlled by the regulator of G protein signaling (RGS) proteins. In this study, we show that RGS protein/Galphai2 interactions are essential for normal thymocyte egress, T cell trafficking, and homeostasis. Mature thymocytes with a Galphai2 mutation that disables RGS protein binding accumulated in the perivascular channels of thymic corticomedullary venules. Severe reductions in peripheral naive CD4+ T cells and regulatory T cells occurred. The mutant CD4+ T cells adhered poorly to high endothelial venules and exhibited defects in lymph node entrance and egress. The kinetics of chemokine receptor signaling were disturbed, including chemokine- induced integrin activation. Despite the thymic and lymph node egress defects, sphingosine-1-phosphate signaling was not obviously perturbed. This study reveals how RGS proteins modulate Galphai2 signaling to facilitate thymocyte egress and T cell trafficking. |
