ArticleThe Journal of biological chemistry2011
A distal enhancer in Il12b is the target of transcriptional repression by the STAT3 pathway and requires the basic leucine zipper (B-ZIP) protein NFIL3.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- The transcription factor NFIL3 drives innate lymphoid cell specification from lymphoid progenitors.Immunity · 2025Article
- Mechanisms of Interleukin-10-Mediated Immunosuppression in Viral Infections.Pathogens (Basel, Switzerland) · 2025Review
- IL-10 targets IRF transcription factors to suppress IFN and inflammatory response genes by epigenetic mechanisms.Nature immunology · 2025Article
- Case report: A special case of pneumonia with a novel STAT3 mutation and Talaromyces marneffei infection.Respiratory medicine case reports · 2025Article
- A pan-cancer characterization of immune-related NFIL3 identifies potential predictive biomarker.Journal of Cancer · 2024Article
- Identification of Cellular Interactions in the Tumor Immune Microenvironment Underlying CD8 T Cell Exhaustion.bioRxiv : the preprint server for biology · 2023Article
- Myeloid-intrinsic cell cycle-related kinase drives immunosuppression to promote tumorigenesis.iScience · 2023Article
- A new border for circadian rhythm gene NFIL3 in diverse fields of cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Article
- The Sympathetic Nervous System Modulates Cancer Vaccine Activity through Monocyte-Derived Cells.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Transcriptional repression shapes the identity and function of tissue macrophages.FEBS open bio · 2021Review
- Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 to Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution.Pharmacological reviews · 2020Review
- Biology and therapeutic potential of interleukin-10.The Journal of experimental medicine · 2020Review
- VISTA Re-programs Macrophage Biology Through the Combined Regulation of Tolerance and Anti-inflammatory Pathways.Frontiers in immunology · 2020Article
- IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses.eLife · 2019Article
- Immune regulation and cytotoxic T cell activation of IL-10 agonists - Preclinical and clinical experience.Seminars in immunology · 2019Review
- NFIL3 Acts as a Nuclear Factor to Increase Osteosarcoma Progression.BioMed research international · 2019Article
- Relationship of systemic IL-10 levels with proinflammatory cytokine responsiveness and lung function in agriculture workers.Respiratory research · 2018Article
- The STAT3/NFIL3 signaling axis-mediated chemotherapy resistance is reversed by Raddeanin A via inducing apoptosis in choriocarcinoma cells.Journal of cellular physiology · 2018Article
- Chromatin Binding ofFrontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Deregulated IL-12 and IL-23 production from activated myeloid lineage cells is a key driver of numerous T cell-dependent autoimmune and inflammatory diseases. IL-12 and IL-23 share a common p40 subunit encoded by Il12b, which is negatively regulated at the transcriptional level by the STAT3 (signal transducer and activator of transcription 3)-activating anti-inflammatory cytokine IL-10. We found that IL-10 targets an enhancer 10 kb upstream of the Il12b transcriptional start site. Within the enhancer, a single 10-bp site is required for the inhibitory effects of IL-10 and is bound by NFIL3 (nuclear factor, interleukin 3-regulated), a B-ZIP transcription factor. Myeloid cells lacking NFIL3 produce excessive IL-12p40 and increased IL-12p70. Thus, the STAT3-dependent expression of NFIL3 is a key component of a negative feedback pathway in myeloid cells that suppresses proinflammatory responses.
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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.