ArticleNature2009
The AP-1 transcription factor Batf controls T(H)17 differentiation.
Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 375 papers.
What it found
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Who cites it
375 citing papers in PubMed, 638 citations in OpenAlex.
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- Spatial transcriptomics maps early B-cell and T-cell activation in hidradenitis suppurativa.The Journal of investigative dermatology · 2026Article
- Gut-derived, inflammatory ILC2s disseminate type 2 immunity to remote lung in food allergen-challenged mice.Journal of leukocyte biology · 2026Article
- Enhancer hubs govern chromatin topology and Th17 cell identity.bioRxiv : the preprint server for biology · 2026Article
- Cellular antibody affinity-based CRISPR screening identifies JUNB as a broadly acting antiviral factor.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Th17 cells require the DNA repair sensor xeroderma pigmentosum complementation Group C to control oxidative DNA damage in a murine model.Nature communications · 2026Article
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- How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?Results and problems in cell differentiation · 2026Review
- scRegulate: single-cell regulatory-embedded variational inference of transcription factor activity from gene expression.Bioinformatics (Oxford, England) · 2025Article
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Peptide ES15-1 derived from Haemonchus contortus promotes goat Th17 response by regulating the STAT3/RORγt pathway.Veterinary research · 2025Article
- The transcriptional repressor BLIMP1 enforces TCF-1-dependent and -independent restriction of the memory fate of CD8Immunity · 2025Article
- Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
315 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
Activator protein 1 (AP-1, also known as JUN) transcription factors are dimers of JUN, FOS, MAF and activating transcription factor (ATF) family proteins characterized by basic region and leucine zipper domains. Many AP-1 proteins contain defined transcriptional activation domains, but BATF and the closely related BATF3 (refs 2, 3) contain only a basic region and leucine zipper, and are considered to be inhibitors of AP-1 activity. Here we show that Batf is required for the differentiation of IL17-producing T helper (T(H)17) cells. T(H)17 cells comprise a CD4(+) T-cell subset that coordinates inflammatory responses in host defence but is pathogenic in autoimmunity. Batf(-/-) mice have normal T(H)1 and T(H)2 differentiation, but show a defect in T(H)17 differentiation, and are resistant to experimental autoimmune encephalomyelitis. Batf(-/-) T cells fail to induce known factors required for T(H)17 differentiation, such as RORgamma t (encoded by Rorc) and the cytokine IL21 (refs 14-17). Neither the addition of IL21 nor the overexpression of RORgamma t fully restores IL17 production in Batf(-/-) T cells. The Il17 promoter is BATF-responsive, and after T(H)17 differentiation, BATF binds conserved intergenic elements in the Il17a-Il17f locus and to the Il17, Il21 and Il22 (ref. 18) promoters. These results demonstrate that the AP-1 protein BATF has a critical role in T(H)17 differentiation.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.