ArticleNature communications2017
JunB promotes Th17 cell identity and restrains alternative CD4
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
What it found
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Who cites it
102 citing papers in PubMed, 140 citations in OpenAlex.
- Assessment and Clinical Relevance of Serum IL-19 Levels in Psoriasis and Atopic Dermatitis Using a Sensitive and Specific Novel Immunoassay.Scientific reports · 2019Trial
- Review
- Integrated single-cell and spatial transcriptomics reveal stromal-immune-vascular crosstalk in patients with interstitial cystitis/bladder pain syndrome.Experimental & molecular medicine · 2026Article
- SPT6 maintains epidermal homeostasis by inhibiting an NF-κB-positive feedback loop to prevent excessive inflammation.Cellular & molecular immunology · 2026Article
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- Post-Surgical Gut Microbiota Alterations in Pediatric Patients with Intestinal Disorders.Journal of clinical medicine · 2026Review
- Stem cell factor 248 shapes ILC2 transcriptional programs and promotes mucosal inflammation in allergic asthma.Frontiers in immunology · 2026Article
- Identification and Validation of a Two-Gene NK Cell-Related Risk Model for COPD: Integration of Single-Cell and Bulk RNA-Seq Analysis.International journal of chronic obstructive pulmonary disease · 2026Article
- Identification of potential biomarkers related to mannose metabolism in keloids: analysis of integrated bulk RNA-seq and scRNA-seq.Frontiers in immunology · 2026Article
- Article
- Knockdown of JunB alleviates LPS-induced H9C2 cardiomyocyte injury and sepsis-induced myocardial injury by activating the PI3K/Akt/mTOR signaling pathway.BMC cardiovascular disorders · 2025Article
- IL-18 drives the Bhlhe40-mediated pathogenic Th17 cell response and exacerbates autoimmune disease progression.Cellular & molecular immunology · 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
- The transcription factor BATF pioneers the differentiation program of effector CD8Cell reports · 2025Article
- Restriction of innate Tγδ17 cell plasticity by an AP-1 regulatory axis.Nature immunology · 2025Article
- Persistent Activation of Endothelial Cells is Linked to Thrombosis and Inflammation in Cerebral Cavernous Malformation Disease.bioRxiv : the preprint server for biology · 2025Article
- Proteome-wide Mendelian randomization reveals causal associations between plasma proteins and autoimmune thyroid disease.Scientific reports · 2025Article
- Testosterone affects female CD4+ T cells in healthy individuals and autoimmune liver diseases.JCI insight · 2025Article
- JunB is required for CD8+ T cell responses to acute infections.International immunology · 2025Article
42 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
T helper 17 (Th17) cell plasticity contributes to both immunity and autoimmunity; however, the factors that control lineage flexibility are mostly unknown. Here we show the activator protein-1 (AP-1) factor JunB is an essential regulator of Th17 cell identity. JunB activates expression of Th17 lineage-specifying genes and coordinately represses genes controlling Th1 and regulatory T-cell fate. JunB supports Th17 cell identity by regulating key AP-1 complex constituents. In particular, JunB limits the expression of the subset repressor IRF8, and impedes access of JunD to regulatory regions of alternative effector loci. Although dispensable for homeostatic Th17 cell development, JunB is required for induction and maintenance of Th17 effector responses in the inflammatory contexts of both acute infection and chronic autoimmunity in mice. Through regulatory network analysis, we show that JunB is a core regulator of global transcriptional programs that promote Th17 cell identity and restrict alternative CD4
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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.