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• W2888893563 endingPage "2461" @default.
• W2888893563 startingPage "2452" @default.
• W2888893563 abstract "Abstract By binding to its ligand ICAM-1, LFA-1 is known to mediate both adhesion and costimulatory signaling for T cell activation. The constitutively high LFA-1 cell surface expression of invariant NKT (iNKT) cells has been shown to be responsible for their distinctive tissue homing and residency within ICAM-rich endothelial vessels. However, the functional impact of LFA-1 on the activation of iNKT cells and other innate T lymphocyte subsets has remained largely unexplored. In particular, it is not clear whether LFA-1 contributes to innate-like pathways of T cell activation, such as IFN-γ secretion in response to IL-12. Using a recombinant ICAM-1-Fc fusion protein to stimulate human iNKT cells in the absence of APCs, we show that LFA-1 engagement enhances their IL-12–driven IFN-γ production. Surprisingly, exposure to high densities of ICAM-1 was also sufficient to activate iNKT cell cytokine secretion independently of IL-12 and associated JAK/STAT signaling. LFA-1 engagement induced elevated cytoplasmic Ca2+ and rapid ERK phosphorylation in iNKT cells, and the resulting IFN-γ secretion was dependent on both of these pathways. Analysis of freshly isolated human PBMC samples revealed that a fraction of lymphocytes that showed elevated LFA-1 cell surface expression produced IFN-γ in response to plate-bound ICAM-1–Fc. A majority of the responding cells were T cells, with the remainder NK cells. The responding T cells included iNKT cells, MAIT cells, and Vδ2+ γδ T cells. These results delineate a novel integrin-mediated pathway of IFN-γ secretion that is a shared feature of innate lymphocytes." @default.
• W2888893563 created "2018-09-07" @default.
• W2888893563 creator A5010768212 @default.
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• W2888893563 date "2018-10-15" @default.
• W2888893563 modified "2023-09-27" @default.
• W2888893563 title "LFA-1 Ligation by High-Density ICAM-1 Is Sufficient To Activate IFN-γ Release by Innate T Lymphocytes" @default.
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• W2888893563 doi "https://doi.org/10.4049/jimmunol.1800537" @default.
• W2888893563 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6179935" @default.
• W2888893563 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30171164" @default.
• W2888893563 hasPublicationYear "2018" @default.
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