ArticleInternational immunology2019
BATF2 prevents T-cell-mediated intestinal inflammation through regulation of the IL-23/IL-17 pathway.
Article in International immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 48 citations in OpenAlex.
- Depleting luminal cysteine with engineered bacteroides vulgatus alleviates experimental colitis by suppressing Th17 differentiation through an ATF6-dependent mechanism.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Integrative eQTL and Mendelian Randomization Analyses with Experimental Validation Prioritize Genetic Candidate Biomarkers for Crohn's Disease.Endocrine, metabolic & immune disorders drug targets · 2026Article
- From gut to pancreas: Shared genetic susceptibility and biological convergence in acute pancreatitis and Crohn's disease.PloS one · 2026Article
- BATF2 is a regulator of interferon-γ signaling in astrocytes during neuroinflammation.Cell reports · 2025Article
- Role of the basic leucine zipper transcription factor BATF2 in modulating immune responses and inflammation in health and disease.Journal of leukocyte biology · 2025Review
- BATF2 inhibits the stem cell-like properties and chemoresistance of gastric cancer cells through PTEN/AKT/β-catenin pathway.Theranostics · 2024Article
- Comprehensive multi-omics analysis of pyroptosis for optimizing neoadjuvant immunotherapy in patients with gastric cancer.Theranostics · 2024Article
- BATF2 enhances proinflammatory cytokine responses in macrophages and improves early host defense against pulmonaryAmerican journal of physiology. Lung cellular and molecular physiology · 2023Article
- The Role of IL-23 in the Pathogenesis and Therapy of Inflammatory Bowel Disease.International journal of molecular sciences · 2023Review
- BATF2 promotes HSC myeloid differentiation by amplifying IFN response mediators during chronic infection.iScience · 2023Article
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- Identifying key genes in CD4Frontiers in genetics · 2022Article
- BATF2 and PDK4 as diagnostic molecular markers of sarcoidosis and their relationship with immune infiltration.Annals of translational medicine · 2022Article
- Comprehensive Transcriptomic Analysis Identifies Novel Antiviral Factors Against Influenza A Virus Infection.Frontiers in immunology · 2021Article
- mMolecular cancer · 2020Article
- SARI prevents ocular angiogenesis and inflammation in mice.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inappropriate activation of the IL-23 signaling pathway causes chronic inflammation through the induction of immunopathological Th17 cells in several tissues including the intestine, whereas adequate Th17 responses are essential for host defense against harmful organisms. In the intestinal lamina propria, IL-23 is primarily produced by innate myeloid cells including dendritic cells (DCs) and macrophages (Mϕs). However, the molecular mechanisms underlying the regulation of IL-23 production by these cells remains poorly understood. In this study, we demonstrated that BATF2 regulates intestinal homeostasis by inhibiting IL-23-driven T-cell responses. Batf2 was highly expressed in intestinal innate myeloid subsets, such as monocytes, CD11b+ CD64+ Mϕs and CD103+ DCs. Batf2-/- mice spontaneously developed colitis and ileitis with altered microbiota composition. In this context, IL-23, but not TNF-α and IL-10, was produced in high quantities by intestinal CD11b+ CD64+ Mϕs from Batf2-/- mice compared with wild-type mice. Moreover, increased numbers of IFN-γ+, IL-17+ and IFN-γ+ IL-17+ CD4+ T cells, but not IL-10+ CD4+ T cells, accumulated in the colons and small intestines of Batf2-/- mice. In addition, RORγt-expressing innate lymphoid cells were increased in Batf2-/- mice. Batf2-/-Rag2-/- mice showed a reduction in intestinal inflammation present in Batf2-/- mice. Furthermore, the high numbers of intestinal IL-17+ and IFN-γ+ IL-17+ CD4+ T cells were markedly reduced in Batf2-/- mice when introducing Il23a deficiency, which was associated with the abrogation of intestinal inflammation. These results indicated that BATF2 in innate myeloid cells is a key molecule for the suppression of IL-23/IL-17 pathway-mediated adaptive intestinal pathology.
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