ArticleScience advances2026
Aryl hydrocarbon receptor deficiency triggers the activation of γδT17 cells to exacerbate autoimmune inflammation.
Article in Science advances, 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
Despite the well-established role of interleukin-17 (IL-17)-producing γδ T cells (γδT17 cells) in autoimmune inflammations, key factors to trigger the activation of γδT17 cells remain largely unknown. Here, we show that aryl hydrocarbon receptor (AhR) is markedly reduced upon γδT17 cell activation. AhR deficiency and pharmacological activation promotes and suppresses γδT17 cell activation, respectively. Mechanistically, AhR deficiency strengthens heat shock protein family A member 9 (HSPA9)-mediated competition with F-box and WD-40 domain protein 11(FBXW11) for binding to RBP-j-associated molecule (RAM) domain of Notch intracellular domain (NICD), which impairs FBXW11-dependent NICD ubiquitination to increase NICD occupancy at the
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