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NKG2D receptors induced by IL-15 costimulate CD28-negative effector CTL in the tissue microenvironment.
TCR specificity dictates CD94/NKG2A expression by human CTL.
Coordinated induction by IL15 of a TCR-independent NKG2D signaling pathway converts CTL into lymphokine-activated killer cells in celiac disease.
Human CD8+ intraepithelial lymphocytes: a unique model to study the regulation of effector cytotoxic T lymphocytes in tissue.
Cytosolic PLA2 is required for CTL-mediated immunopathology of celiac disease via NKG2D and IL-15.
NKG2 receptor-mediated regulation of effector CTL functions in the human tissue microenvironment.
Reprogramming of CTLs into natural killer-like cells in celiac disease.
Distinct and Synergistic Contributions of Epithelial Stress and Adaptive Immunity to Functions of Intraepithelial Killer Cells and Active Celiac Disease.
Cysteinyl leukotrienes mediate lymphokine killer activity induced by NKG2D and IL-15 in cytotoxic T cells during celiac disease.
Tissue alarmins and adaptive cytokine induce dynamic and distinct transcriptional responses in tissue-resident intraepithelial cytotoxic T lymphocytes.
Tet2 deficiency drives liver microbiome dysbiosis triggering Tc1 cell autoimmune hepatitis.
T Lymphocytes Cytotoxic