ArticleNature communications2026
Cell type-specific enhancers regulate IL-22 expression in innate and adaptive type 3 lymphoid cells.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- High-resolution promoter interaction analysis implicates genes involved in activation of type 3 innate lymphoid cells in immune disease risk.Nature genetics · 2026Article
- High-resolution promoter interaction analysis implicates genes involved in the activation of Type 3 Innate Lymphoid Cells in autoimmune disease risk.bioRxiv : the preprint server for biology · 2026Article
- mtROS-NF-κB signaling supports ILC3 function and survival during sepsis-induced intestinal injury.Frontiers in immunology · 2026Article
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Abstract
IL-22, a signature cytokine for type 3 lymphoid cells, including T helper 17/22 (Th17/22) and type 3 innate lymphoid cells (ILC3), mediates epithelial homeostasis and protective pathogen responses in barrier tissues. Upon dysregulation, IL-22 can drive chronic inflammatory diseases, yet little is known about transcriptional elements modulating its expression. Here, we identify two enhancers, E22-1 and E22-2, with distinct capacities for regulating Il22 expression in type 3 lymphoid cells. Both enhancers are necessary for protection from Citrobacter rodentium infection and for the onset of IL-22-mediated psoriasis. E22-2 is specifically required for IL-22 expression in ILC3s, while E22-1 functions in both Th17/22 and ILC3. The ILC3 specificity of E22-2 is attributed to the presence of multiple Runx3 sites and the lack of a functional RORγt motif. We conclude that Th17/22 and ILC3 cells use distinct cis-elements to differentially regulate IL-22 expression, while orchestrating homeostatic protection and pathogen defense in barrier tissues.
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