AF6 orchestrates macrophage polarization via JAK2-STAT3 signaling and supports intestinal regeneration by stimulating stem cell proliferation

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AF6 is identified as a key regulator of pro-inflammatory macrophage polarization in a DSS-induced colitis model.
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Deletion of AF6 in macrophages impairs JAK-STAT3 signaling and shifts polarization away from pro-inflammatory M1.
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AF6-deficient macrophages enhance epithelial regeneration through increased IL-10 production and Wnt/β-catenin activation.
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The study highlights the AF6-JAK2-STAT3 axis as a potential therapeutic target for managing colitis.
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AF6 functions as a scaffold protein that organizes signaling complexes, influencing macrophage activation and intestinal inflammation.

Frontiers In Immunology

by Tao Jian, Xiaoxia Dong, Jingwen Kong, Xinyu Wang, Meiyan Qi, Lixing Zhan, Lilei Zhuang
June 19, 2026

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