Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease.
By B. Meresse, Zhangguo Chen, C. Ciszewski, M. Tretiakova, G. Bhagat, T. Krausz, D. Raulet, L. Lanier, V. Groh, T. Spies and 3 more. Immunity, 2004
889 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/53a32217d0689061d04f2e9ffa910812e22a2a32
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In Immunology
Citations in the corpus
- The light and dark sides of intestinal intraepithelial lymphocytes (2011, positive): “In this setting, TCR-activated CD8αβ + TCRαβ + induced IELs cause severe villous atrophy by targeting intestinal epithelial cells that express stress-induced MHC class I polypeptide-related sequence (MIC) antigens, in an NKG2D-dependent fashio”
- Regulation of ligands for the NKG2D activating receptor (2013, background): “In some scenarios, such as after potent activation of human CD8+ T cells with IL15 and CD3 engagement, subsequent NKG2D engagement in the absence of T cell receptor activation is sufficient to trigger target cell killing (18).”
- Up on the tightrope: natural killer cell activation and inhibition (2008, background): “Similarly, the ability of human CD8 + T cells to kill when activated through the NKG2D receptor also requires previous stimulation by high concentrations of IL-2 or IL-15 (ref”
- Wheat seed storage proteins: Advances in molecular genetics, diversity and breeding applications (2014, background): “In addition to the adaptive CD4þ T cell response to gluten, CD is characterized by upregulation of IL-15, an intraepithelial T cell infiltrate expressing the NKG2D receptor, and the overexpression of a ligand for NKG2D (MICA) (Meresse et al., 2004).”
- CD49a Expression Defines Tissue-Resident CD8+ T Cells Poised for Cytotoxic Function in Human Skin (2017, neutral): “lymphocyte responses that turn pathological in celiac disease (Meresse et al., 2004).”
- Cytokines in Cancer Immunotherapy (2011, background): “These effects are mediated through direct activation of CD8+ effector T cells in an antigenindependent manner [103].”