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- W4313354647 abstract "Abstract Mucosal innate lymphocyte subsets have emerged as an important new factor in CD pathogenesis, but the role of NK cells is poorly understood. A recent genetic study identified the KIR gene KIR2DL2/3 as a risk factor for CD in the genetic context of its ligand HLA-C1. However, the biologic mechanism of this genetic contribution is unknown. NK cells are mainly known for their cytolytic function, but recent work indicates that strong KIR/HLA interactions that induce NK “licensing” augment NK cytotoxicity but also IFN-γ production. We therefore tested the hypothesis that human NK licensing by KIR2DL2/3 and HLA-C1 induces a broader cytokine program that modifies the threshold of pro-inflammatory T cell activation. Single cell multiplex functional proteomics revealed that licensed and unlicensed NK cells had strikingly distinct cytokine programs. Licensed NK cells were distinguished by high-output, proinflammatory, poly-cytokine expression. Select cytokine among this output fully accounted for their unique capacity, unlike unlicensed NK cells, to efficiently augment antigenic CD4+ T cell proliferation and induce CD4+ T cell IL-17A production. In conclusion, NK licensing mediated by KIR2DL2/3 and HLA-C1 elicits a novel cytokine program of NK cells that activates and induces pro-inflammatory CD4+ T cells, and therefore provides a predisposing biologic mechanism for this KIR-associated susceptibility to CD and other chronic inflammatory syndromes." @default.
- W4313354647 created "2023-01-06" @default.
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- W4313354647 date "2013-05-01" @default.
- W4313354647 modified "2023-09-27" @default.
- W4313354647 title "Genetically-determined cytokine programs of human NK cells uncover a novel mechanism of NK cells and Killer cell IgG-like Receptor genes in Crohn’s Disease susceptibility (P3262)" @default.
- W4313354647 doi "https://doi.org/10.4049/jimmunol.190.supp.136.13" @default.
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