| First Author | Tomassian T | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 6 | Pages | 2993-3002 |
| PubMed ID | 21849673 | Mgi Jnum | J:179237 |
| Mgi Id | MGI:5301491 | Doi | 10.4049/jimmunol.1101447 |
| Citation | Tomassian T, et al. (2011) Caveolin-1 orchestrates TCR synaptic polarity, signal specificity, and function in CD8 T cells. J Immunol 187(6):2993-3002 |
| abstractText | TCR engagement triggers the polarized recruitment of membrane, actin, and transducer assemblies within the T cell-APC contact that amplify and specify signaling cascades and T effector activity. We report that caveolin-1, a scaffold that regulates polarity and signaling in nonlymphoid cells, is required for optimal TCR-induced actin polymerization, synaptic membrane raft polarity, and function in CD8, but not CD4, T cells. In CD8(+) T cells, caveolin-1 ablation selectively impaired TCR-induced NFAT-dependent NFATc1 and cytokine gene expression, whereas caveolin-1 re-expression promoted NFATc1 gene expression. Alternatively, caveolin-1 ablation did not affect TCR-induced NF-kappaB-dependent Ikappabalpha expression. Cav-1(-/-) mice did not efficiently promote CD8 immunity to lymphocytic choriomeningitis virus, nor did cav-1(-/-) OT-1(+) CD8(+) T cells efficiently respond to Listeria monocytogenes-OVA after transfer into wild-type hosts. Therefore, caveolin-1 is a T cell-intrinsic orchestrator of TCR-mediated membrane polarity and signal specificity selectively employed by CD8 T cells to customize TCR responsiveness. |
