有哪些信誉好的足球投注网站cytotoxicity of cd56bright nk cells towards autologous activated cd4+ t cells is mediated through nkg2d, lfa-1 and trail and dampened via cd94nkg2acd56bright nk细胞的细胞毒性对自体激活通过nkg2d cd4 + t细胞是介导,通过cd94nkg2a lfa-1小道和抑制.pdfVIP
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cytotoxicityofcd56brightnkcellstowardsautologousactivatedcd4tcellsismediatedthroughnkg2d,lfa-1andtrailanddampenedviacd94nkg2acd56brightnk细胞的细胞毒性对自体激活通过nkg2dcd4t细胞是介导,通过cd94nkg2alfa-1小道和抑制
Cytotoxicity of CD56bright NK Cells towards Autologous Activated CD4+ T Cells Is Mediated through NKG2D, LFA- 1 and TRAIL and Dampened via CD94/NKG2A 1,4 3 2 4 1 Natasja Nielsen , Niels Ødum , Birgitte Ursø , Lewis L. Lanier , Pieter Spee * ˚ ˚ 1Translational Immunology, Novo Nordisk A/S, Maløv, Denmark, 2 Monocyte Biology, Inflammation Biology, Novo Nordisk A/S, Maløv, Denmark, 3 Department of Biology, Faculty of Science, University of Copenhagen, Copenhagen, Denmark, 4 Department of Microbiology and Immunology and the Cancer Research Institute, University of California San Francisco, San Francisco, California, United States of America Abstract In mouse models of chronic inflammatory diseases, Natural Killer (NK) cells can play an immunoregulatory role by eliminating chronically activated leukocytes. Indirect evidence suggests that NK cells may also be immunoregulatory in humans. Two subsets of human NK cells can be phenotypically distinguished as CD16+CD56dim and CD16dim/ 2CD56bright. An expansion in the CD56bright NK cell subset has been associated with clinical responses to therapy in various autoimmune diseases, suggesting an immunoregulatory role for this subset in vivo. Here we compared the regulation of activated human CD4+ T cells by CD56dim and CD56bright autologous NK cells in vitro. Both subsets efficiently killed activated, but not resting, CD4+ T cells. The activating receptor NKG2D, as well as the integrin LFA-1 and the TRAIL pathway, played important roles in this process. Degranulation by NK cells towards activated CD4+ T cells was enhanced by IL-2, IL-15, IL-12+IL-18 and IFN-a.
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