ArticleBMC immunology2026
CD30 knockout attenuates experimental colitis by reducing inflammatory cytokine production.
Article in BMC 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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Abstract
backgroundInflammatory bowel disease (IBD) is characterized by dysregulated T helper immune responses. Crohn’s disease is predominantly associated with excessive Th1 and Th17 responses, while ulcerative colitis displays a more heterogeneous immune profile. However, the molecular mechanisms underlying Th1 cell differentiation in intestinal inflammation remain incompletely understood. CD30, a member of the tumor necrosis factor receptor superfamily, has been implicated in various inflammatory conditions, yet its role in IBD pathogenesis has not been fully elucidated.
objectivesThis study aimed to investigate the role of CD30 in experimental colitis and its regulation of Th1 cell differentiation through the NF-κB signaling pathway.
methodsAcute colitis was induced in wild-type and CD30-deficient mice using 3% dextran sulfate sodium (DSS) for 7 days. CD30 expression in colonic tissues was assessed by immunohistochemistry, quantitative real-time PCR, and Western blot. Naive CD4 + T cells were isolated and stimulated under Th1-polarizing conditions with or without CD30 knockdown using small interfering RNA. Th1 differentiation was evaluated by flow cytometry with verification using T-bet and IL-17 A staining, and related transcription factors and cytokines were measured. The NF-κB signaling pathway was examined in lipopolysaccharide (LPS)-stimulated conditions.
resultsCD30 expression was significantly upregulated in DSS-induced colitis, correlating with increased Th1 markers including T-bet and IFN-γ. In vitro, CD30 knockdown markedly suppressed Th1 cell differentiation from naive CD4 + T cells, reducing IFN-γ + cell proportions among CD4 + T cells and downregulating T-bet, STAT4, and IL-12Rβ2 expression. Mechanistically, CD30 deficiency inhibited NF-κB pathway activation by reducing p65 phosphorylation and preventing IκBα degradation. In vivo, CD30-/- mice exhibited attenuated colitis severity with reduced disease activity index, improved colon length, decreased histological damage, and diminished Th1 cytokine production compared to wild-type littermates.
conclusionsCD30 promotes Th1 cell differentiation and exacerbates experimental colitis through NF-κB-dependent mechanisms. These findings identify CD30 as a potential therapeutic target for IBD treatment.
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