ArticleFrontiers in immunology2026
IL-23 and monocyte interactions redirect human Th17.1 cells to an IL-17A
Article 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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Abstract
Introduction: IL-23-targeted therapies have demonstrated clinical efficacy in psoriatic arthritis (PsA), primarily through the reduction of IL-17A-driven inflammation. Consequently, most studies have focused on classical, high IL-17A-producing, CCR6 Methods: Peripheral blood mononuclear cells (PBMCs) from treatment-naive patients with early PsA were stimulated in the presence of IL-23 or anti-IL-23 antibody before quantifying IL-17A and IFN-γ secretion. Additionally, human memory CCR6 Results: As expected, IL-23 stimulation induced IL-17A in PsA PBMCs, whereas IL-23 inhibition reduced IL-17A secretion but did not affect IFN-γ. In healthy donor PBMCs, ex vivo IL-23R expression was restricted to memory CCR6 Conclusion: IL-23 exerts distinct effects on Th17.1 compared to Th17 cells. We show a role for IL-23 in IFN-γ upregulation in Th17.1 cells, which is reversed in the presence of monocytes. In co-culture with monocytes, Th17.1 cells progress to a pathogenic IL-17A
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