期刊
JOURNAL OF IMMUNOLOGY
卷 187, 期 6, 页码 2993-3002出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1101447
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资金
- Microbial Pathogenesis Training Grant [2-T32-AI-07323, T32-AI07323-15]
- Arthritis Foundation
- Clinical and Fundamental Training Grant [AI07126-30]
- Warsaw Fellowship
- National Institutes of Health [R01-AI067253-10, AI085043]
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-kappa B-dependent I kappa b alpha 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. The Journal of Immunology, 2011, 187: 2993-3002.
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