ArticleJournal of immunology (Baltimore, Md. : 1950)2014
The transcription factor E74-like factor 4 suppresses differentiation of proliferating CD4+ T cells to the Th17 lineage.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- A novel ELF4 gene variant disrupts T and NK cell function in a patient with immune thrombocytopenia (ITP).Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A truncatingFrontiers in immunology · 2026Article
- Review
- Novel pathogenic variant in the deficiency in ELF4, X-linked (DEX): case report and literature review.Orphanet journal of rare diseases · 2025Review
- ELF4 improves sepsis-induced myocardial injury by regulating STING signaling-mediated T cells differentiation.Cell biology and toxicology · 2025Article
- Transcription factor ELF4 in physiology and diseases: Molecular roles and clinical implications.Genes & diseases · 2025Review
- A Novel Frameshift Variant of the ELF4 Gene in a Patient with Autoinflammatory Disease: Clinical Features, Transcriptomic Profiling and Functional Studies.Journal of clinical immunology · 2024Article
- [Two Cases of Behcet's Disease-Like Syndrome with Gene Deficiency inSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- Current understanding of ELF4 deficiency: a novel inborn error of immunity.World journal of pediatrics : WJP · 2024Review
- "Deficiency in ELF4, X-Linked": a Monogenic Disease Entity Resembling Behçet's Syndrome and Inflammatory Bowel Disease.Journal of clinical immunology · 2024Article
- ELF4 was a prognostic biomarker and related to immune infiltrates in glioma.Journal of Cancer · 2024Article
- Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress.BMC molecular and cell biology · 2023Article
- In vitro treatment of murine splenocytes with extracellular vesicles derived from mesenchymal stem cells altered the mRNA levels of the master regulator genes of T helper cell subsets.Molecular biology reports · 2023Article
- The transcription factor ELF4 alleviates inflammatory bowel disease by activating IL1RN transcription, suppressing inflammatory TH17 cell activity, and inducing macrophage M2 polarization.Frontiers in immunology · 2023Article
- Loss of Function Mutation in ELF4 Causes Autoinflammatory and Immunodeficiency Disease in Human.Journal of clinical immunology · 2022Article
- Immune Response of an OralViruses · 2022Article
- Proximal and Distal Regions of Pathogenic Th17 Related Chromatin Loci Are Sequentially Accessible During Pathogenicity of Th17.Frontiers in immunology · 2022Article
- Human autoinflammatory disease reveals ELF4 as a transcriptional regulator of inflammation.Nature immunology · 2021Article
- Immunosuppressive Effects of Mesenchymal Stem Cells-derived Exosomes.Stem cell reviews and reports · 2021Review
- Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The differentiation of CD4(+) T cells into different Th lineages is driven by cytokine milieu in the priming site and the underlying transcriptional circuitry. Even though many positive regulators have been identified, it is not clear how this process is inhibited at transcriptional level. In this study, we report that the E-twenty six (ETS) transcription factor E74-like factor 4 (ELF4) suppresses the differentiation of Th17 cells both in vitro and in vivo. Culture of naive Elf4(-/-) CD4(+) T cells in the presence of IL-6 and TGF-β (or IL-6, IL-23, and IL-1β) resulted in increased numbers of IL-17A-positive cells compared with wild-type controls. In contrast, the differentiation to Th1, Th2, or regulatory T cells was largely unaffected by loss of ELF4. The increased expression of genes involved in Th17 differentiation observed in Elf4(-/-) CD4(+) T cells suggested that ELF4 controls their programming into the Th17 lineage rather than only IL-17A gene expression. Despite normal proliferation of naive CD4(+) T cells, loss of ELF4 lowered the requirement of IL-6 and TGF-β signaling for IL-17A induction in each cell division. ELF4 did not inhibit Th17 differentiation by promoting IL-2 production as proposed for another ETS transcription factor, ETS1. Elf4(-/-) mice showed increased numbers of Th17 cells in the lamina propria at steady state, in lymph nodes after immunization, and, most importantly, in the CNS following experimental autoimmune encephalomyelitis induction, contributing to the increased disease severity. Collectively, our findings suggest that ELF4 restrains Th17 differentiation in dividing CD4(+) T cells by regulating commitment to the Th17 differentiation program.
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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.