ArticleThe Journal of biological chemistry2016
The Atypical Inhibitor of NF-κB, IκBζ, Controls Macrophage Interleukin-10 Expression.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- IκBζ target genes in chronic lymphocytic leukemia.iScience · 2026Article
- Signal-integrated control of immune and reparative programs establishes blood-derived fibrocytes reprogrammable toward induced pluripotency.Biology open · 2026Article
- IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Macrophages tune responses to pathogen dynamics through TLR4 stimulation memory and by licensing susceptibility to IL-10.bioRxiv : the preprint server for biology · 2026Article
- WNT16 from decidual stromal cells orchestrates M2 macrophage polarization via β-catenin signaling and chromatin remodeling at the maternal-fetal interface.Frontiers in immunology · 2025Article
- Laminin-derived peptide, IKVAV, modulates macrophage phenotype through integrin mediation.Matrix biology plus · 2024Article
- Codonopsis pilosula-derived glycopeptide dCP1 promotes the polarization of tumor-associated macrophage from M2-like to M1 phenotype.Cancer immunology, immunotherapy : CII · 2024Article
- IκBζ is a dual-use coactivator of NF-κB and POU transcription factors.Molecular cell · 2024Article
- Methylglyoxal suppresses microglia inflammatory response through NRF2-IκBζ pathway.Redox biology · 2023Article
- The central inflammatory regulator IκBζ: induction, regulation and physiological functions.Frontiers in immunology · 2023Review
- Inflammation suppresses DLG2 expression decreasing inflammasome formation.Journal of cancer research and clinical oncology · 2022Article
- Spatially resolved deconvolution of the fibrotic niche in lung fibrosis.Cell reports · 2022Article
- MiR-25 blunts autophagy and promotes the survival ofiScience · 2022Article
- Article
- Chromatin accessibility analysis identifies the transcription factor ETV5 as a suppressor of adipose tissue macrophage activation in obesity.Cell death & disease · 2021Article
- Signaling pathways in the regulation of cytokine release syndrome in human diseases and intervention therapy.Signal transduction and targeted therapy · 2021Review
- Upregulation of NFKBIZ affects bladder cancer progression via the PTEN/PI3K/Akt signaling pathway.International journal of molecular medicine · 2021Article
- Regulation of theInfection and immunity · 2021Article
- Network Pharmacology Analysis of the Therapeutic Mechanisms Underlying Beimu-Gualou Formula Activity against Bronchiectasis withEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Nociceptive related microRNAs and their role in rheumatoid arthritis.Molecular biology reports · 2020Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages constitute a first line of pathogen defense by triggering a number of inflammatory responses and the secretion of various pro-inflammatory cytokines. Recently, we and others found that IκBζ, an atypical IκB family member and transcriptional coactivator of selected NF-κB target genes, is essential for macrophage expression of a subset of pro-inflammatory cytokines, such as IL-6, IL-12, and CCL2. Despite defective pro-inflammatory cytokine expression, however, IκBζ-deficient mice develop symptoms of chronic inflammation. To elucidate this discrepancy, we analyzed a regulatory role of IκBζ for the expression of anti-inflammatory cytokines and identified IκBζ as an essential activator of IL-10 expression. LPS-challenged peritoneal and bone marrow-derived macrophages from IκBζ-deficient mice revealed strongly decreased transcription and secretion of IL-10 compared with wild-type mice. Moreover, ectopic expression of IκBζ was sufficient to stimulate Il10 transcription. On the molecular level, IκBζ directly activated the Il10 promoter at a proximal κB site and was required for the transcription-enhancing trimethylation of histone 3 at lysine 4. Together, our findings show for the first time the IκBζ-dependent expression of an anti-inflammatory cytokine that is crucial in controlling immune responses.
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