| First Author | Borger JG | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 3 | Pages | 874-884 |
| PubMed ID | 28637901 | Mgi Jnum | J:250894 |
| Mgi Id | MGI:6099305 | Doi | 10.4049/jimmunol.1700431 |
| Citation | Borger JG, et al. (2017) Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells. J Immunol 199(3):874-884 |
| abstractText | TCR stimulation by peptide-MHC complexes on APCs requires precise reorganization of molecules into the area of cellular contact to form an immunological synapse from where T cell signaling is initiated. Caveolin (Cav)1, a widely expressed transmembrane protein, is involved in the regulation of membrane composition, cellular polarity and trafficking, and the organization of signal transduction pathways. The presence of Cav1 protein in T cells was identified only recently, and its function in this context is not well understood. We show that Cav1-knockout CD8 T cells have a reduction in membrane cholesterol and sphingomyelin, and upon TCR triggering they exhibit altered morphology and polarity, with reduced effector function compared with Cav1 wild-type CD8 T cells. In particular, redistribution of the beta2 integrin LFA-1 to the immunological synapse is compromised in Cav1-knockout T cells, as is the ability of LFA-1 to form high-avidity interactions with ICAM-1. Our results identify a role for Cav1 in membrane organization and beta2 integrin function in primary CD8 T cells. |
