ArticleMucosal immunology2014
Transcription of RORγt in developing Th17 cells is regulated by E-proteins.
Article in Mucosal immunology, 2014. 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, 32 citations in OpenAlex.
- TGF-β Regulation of T Cells.Annual review of immunology · 2023Review
- Regulation of the Signal-Dependent E Protein HEBAlt Through a YYY Motif Is Required for Progression Through T Cell Development.Frontiers in immunology · 2022Article
- Signaling networks controlling ID and E protein activity in T cell differentiation and function.Frontiers in immunology · 2022Review
- Proximal and Distal Regions of Pathogenic Th17 Related Chromatin Loci Are Sequentially Accessible During Pathogenicity of Th17.Frontiers in immunology · 2022Article
- The Pathogenic Roles of IL-22 in Colitis: Its Transcription Regulation by Musculin in T Helper Subsets and Innate Lymphoid Cells.Frontiers in immunology · 2021Article
- Interleukin-6 (IL-6) Activates the NOTCH1 Signaling Pathway Through E-Proteins in Endometriotic Lesions.The Journal of clinical endocrinology and metabolism · 2020Article
- NFAT primes the human RORC locus for RORγt expression in CD4Nature communications · 2019Article
- Oxysterol levels and metabolism in the course of neuroinflammation: insights from in vitro and in vivo models.Journal of neuroinflammation · 2018Article
- HEB is required for the specification of fetal IL-17-producing γδ T cells.Nature communications · 2017Article
- Regulatory T cells characterized by low Id3 expression are highly suppressive and accumulate during chronic infection.Oncotarget · 2017Article
- Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease.Frontiers in immunology · 2017Review
- Upregulation of CD4+T-Cell Derived MiR-223 in The Relapsing Phase of Multiple Sclerosis Patients.Cell journal · 2016Article
- Jieduquyuziyin prescription suppresses IL-17 production and Th17 activity in MRL/lpr mice by inhibiting expression of Ca(2+)/calmodulin-dependent protein kinase-4.Journal of natural medicines · 2015Article
- Article
- Orchestration of invariant natural killer T cell development by E and Id proteins.Critical reviews in immunology · 2015Review
- Complex interactions of transcription factors in mediating cytokine biology in T cells.Immunological reviews · 2014Review
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In the present study we investigated the molecular mechanisms regulating the expression of RAR-related orphan receptor gamma t (RORγt), the central factor controlling interleukin (IL)-17 transcription and Th17 differentiation. In key studies, we found that cells from mice with major deletions of E-protein transcription factors, E2A and HEB, display greatly reduced RORγt/IL-17 expression and that E-protein-deficient mice exhibit greatly diminished IL-17-dependent inflammation in experimental allergic encephalitis models. In additional studies, we unexpectedly found that cells from mice with deletion of Id3, a protein that inhibits E-protein binding to DNA, display diminished RORγt/IL-17 expression and mice deficient in this protein exhibit decreased Th17-mediated inflammation in a cell-transfer colitis model. The explanation of these initially paradoxical findings came from studies showing that Id3 deficiency leads to increased IL-4-induced GATA-3 expression, the latter a negative regulator of RORγt transcription; thus, increased Id3 expression likely has a net positive effect on RORγt expression via its inhibition of IL-4 production. Finally, we found that both E-proteins and Id3 are upregulated in tandem by the cytokines that induce Th17 differentiation, transforming growth factor-β, and IL-6, implying that these transcription factors are critical regulators of Th17 induction.
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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.