Journal
JOURNAL OF IMMUNOLOGY
Volume 199, Issue 3, Pages 874-884Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1700431
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Funding
- Medical Research Council [G1100116]
- Wellcome Trust [095831, WT096669AIA]
- Biotechnology and Biological Sciences Research Council
- Academy of Finland
- Sigrid Juselius Foundation
- Medical Research Council [G1100116] Funding Source: researchfish
- MRC [G1100116] Funding Source: UKRI
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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 b2 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 b2 integrin function in primary CD8 T cells.
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