ArticleBlood research2025
STING-Dependent spontaneous platelet adhesion potentiates NK cell proinflammatory responses in pediatric crohn's disease.
Article in Blood research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
backgroundPlatelets are hypothesized to participate in the pathogenesis of Crohn's disease (CD) by interacting with other inflammatory cells such as natural killer (NK) cells. In this study, we aimed to evaluate the effects of platelet-NK cell interactions, both in vitro and in vivo, along with the corresponding mechanisms.
methodsClinical data were collected from patients with CD and IL-10 receptor alpha (IL-10RA) mutations, with the control group being comprised of patients with functional abdominal pain. Platelets and NK cells from the patients' colon tissues were immunostained. Dextran sulfate sodium (DSS)-induced colitis models using wild type (WT) and Stimulator of Interferon Genes knockout (STING
resultsCirculating and intestinal platelets were higher in patients with IL-10RA mutations compared to CD patients and correlated positively with serum cytokines, fecal calprotectin (FCP), and blood NK cells. Gut inflammation and T3 cytokine expression in NK cells were significantly lower in STING
conclusionsSpontaneous platelet adhesion via STING signaling potentiates NK cell proinflammatory response in CD.
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