ReviewFrontiers in immunology2026
IL-37 and IL-38 in sepsis: immune-metabolic rheostats in a dynamic inflammatory continuum.
Review in Frontiers in immunology, 2026. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
10 authors.
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Abstract
Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection, characterised by dynamic and overlapping phases of hyperinflammation and immune suppression. Despite advances in critical care, effective immunomodulatory therapies remain lacking, reflecting an incomplete understanding of its complex immunopathology. Central to sepsis progression is the cytokine storm, a transient but dominant inflammatory surge that contributes to endothelial injury, microvascular dysfunction, and multi-organ failure, followed in some patients by compensatory immunosuppression. Within this evolving immunological landscape, IL-37 and IL-38 have emerged as key members of the IL-1 cytokine family with context-dependent immunoregulatory functions. IL-37 broadly suppresses NF-κB- and MAPK-mediated inflammatory signalling and reprogrammes immunometabolism
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