ArticleFrontiers in immunology2026
AF6 orchestrates macrophage polarization via JAK2-STAT3 signaling and supports intestinal regeneration by stimulating stem cell proliferation.
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: Macrophages play a central role in regulating intestinal inflammation, resolution, and tissue repair. However, the upstream regulators that govern their polarization during colitis remain poorly defined. Methods: In this study, we used a dextran sulfate sodium (DSS)-induced colitis model to investigate the role of the scaffold protein AF6 in colitis pathogenesis. Results: We identify AF6 as a key regulator that promotes pro-inflammatory macrophage polarization and exacerbates colitis. Mechanistically, AF6 expression promoted JAK-STAT3 complex formation. In turn, its deletion in macrophages resulted in impaired JAK-STAT3 signaling pathway and a shift away from pro-inflammatory M1 polarization. Furthermore, the AF6-deficient macrophages were determined to also promote epithelial regeneration through enhanced IL-10 production and downstream activation of Wnt/β-catenin signaling in intestinal organoids culture. Discussion: Thus, our study defines a therapeutically amenable AF6-JAK2-STAT3 axis that controls macrophage-driven pathogenesis in colitis, revealing a novel strategy to break the cycle of inflammation and impaired repair.
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