Browsing by Subject "NKT"

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    Role of innate T cells in necrotizing enterocolitis
    (Frontiers Media, 2024-02-08) Liu, Jianyun; Joseph, Sharon; Manohar, Krishna; Lee, Jasmine; Brokaw, John P.; Shelley, W. Christopher; Markel, Troy A.; Surgery, School of Medicine
    Necrotizing enterocolitis (NEC) is a destructive gastrointestinal disease primarily affecting preterm babies. Despite advancements in neonatal care, NEC remains a significant cause of morbidity and mortality in neonatal intensive care units worldwide and the etiology of NEC is still unclear. Risk factors for NEC include prematurity, very low birth weight, feeding with formula, intestinal dysbiosis and bacterial infection. A review of the literature would suggest that supplementation of prebiotics and probiotics prevents NEC by altering the immune responses. Innate T cells, a highly conserved subpopulation of T cells that responds quickly to stimulation, develops differently from conventional T cells in neonates. This review aims to provide a succinct overview of innate T cells in neonates, encompassing their phenotypic characteristics, functional roles, likely involvement in the pathogenesis of NEC, and potential therapeutic implications.
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    STAT4 is required for IL-23 responsiveness in Th17 memory cells and NKT cells
    (Taylor & Francis Group, 2014-10-30) Glosson-Byers, Nicole L.; Sehra, Sarita; Kaplan, Mark H.; Department of Pediatrics, School of Medicine
    STAT4 is a critical mediator of inflammatory immunity and is required for all known IL-12 biological responses, including the induction of IFN-γ and development of Th1 cells. We demonstrate that IL-23, an IL-12-related cytokine, also requires STAT4 for optimal IL-17 secretion from memory T helper cells and NKT cells. Although IL-23 stimulation had modest effects on STAT4 activation, STAT4-deficiency results in reduced Il23r expression. These data demonstrate a restricted requirement for STAT4 in innate and adaptive IL-17-secreting T cell responses that might contribute to inflammatory immunity.