ArticleCell reports2023
Kruppel-like factor 2+ CD4 T cells avert microbiota-induced intestinal inflammation.
Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Effect of the intestinal microbiota on TSeminars in immunopathology · 2026Review
- Maternal Krüppel-like factor 2 (KLF2)+ CD4 T cells promote fertility and fetal tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cannabidiol exerts antiinflammatory effects but maintains T effector memory cell differentiation in humans.JCI insight · 2026Article
- Investigating the mechanisms of lactulose on gut health and uric acid metabolism in geese via transcriptomics.Scientific reports · 2025Article
- Disrupted priming within draining lymph nodes drives immune quiescence in gastric cancer.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Intestinal colonization by antigenically foreign microbes necessitates expanded peripheral immune tolerance. Here we show commensal microbiota prime expansion of CD4 T cells unified by the Kruppel-like factor 2 (KLF2) transcriptional regulator and an essential role for KLF2+ CD4 cells in averting microbiota-driven intestinal inflammation. CD4 cells with commensal specificity in secondary lymphoid organs and intestinal tissues are enriched for KLF2 expression, and distinct from FOXP3+ regulatory T cells or other differentiation lineages. Mice with conditional KLF2 deficiency in T cells develop spontaneous rectal prolapse and intestinal inflammation, phenotypes overturned by eliminating microbiota or reconstituting with donor KLF2+ cells. Activated KLF2+ cells selectively produce IL-10, and eliminating IL-10 overrides their suppressive function in vitro and protection against intestinal inflammation in vivo. Together with reduced KLF2+ CD4 cell accumulation in Crohn's disease, a necessity for the KLF2+ subpopulation of T regulatory type 1 (Tr1) cells in sustaining commensal tolerance is demonstrated.
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Registered trials
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