ArticleNature communications2021
The RNase MCPIP3 promotes skin inflammation by orchestrating myeloid cytokine response.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- The regnase family in autoimmune diseases: a regnase-1-centered perspective on cellular heterogeneity.Molecular biology reports · 2026Review
- Article
- A combination therapy strategy: precision co-targeting of CCR7 and JAK1 with a smart hydrogel for inflammatory skin diseases.Journal of nanobiotechnology · 2026Article
- The Regnase pathway: a core axis in immune regulation and inflammatory disease.Frontiers in immunology · 2026Review
- Rewiring tumor immunity via zinc finger proteins: a new frontier in cancer immunotherapy.Journal of translational medicine · 2025Review
- Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- MCPIP3/Regnase-3 binds 14-3-3 proteins and contributes to the regulation of the cell cycle in human immortalized keratinocytes.Scientific reports · 2025Article
- Constitutive expression of the transcriptional co-activator IκBζ promotes melanoma growth and immunotherapy resistance.Nature communications · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- Castleman Disease-Still More Questions than Answers: A Case Report and Review of the Literature.Journal of clinical medicine · 2025Review
- MCPIP3 orchestrates the balance of epidermal proliferation and differentiation.Cell communication and signaling : CCS · 2025Article
- Skin immune microenvironment in psoriasis: from bench to bedside.Frontiers in immunology · 2025Review
- Exploring therapeutic mechanism of Fuzhenghefuzhiyang Formula in psoriasis: inflammation and metabolism regulation.Frontiers in immunology · 2025Article
- The identification of key molecules and pathways in the crosstalk of calcium oxalate-treated TCMK-1 cells and macrophage via exosomes.Scientific reports · 2024Article
- Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Life science alliance · 2024Article
- Regulation of inflammatory diseases via the control of mRNA decay.Inflammation and regeneration · 2024Review
- Regulation of tumor metastasis and CD8Cellular & molecular biology letters · 2024Article
- Cysteine-rich zinc finger proteins and the nuclear factor kappa-B pathway.Frontiers in chemical biology · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCCH zinc finger proteins resolve immune responses by degrading the mRNAs of inflammatory cytokines such as tumor necrosis factor (TNF) and interleukin (IL)-6. Here we report that one such family member, monocyte chemotactic protein-induced protein 3 (MCPIP3, also named ZC3H12C or Regnase-3), promotes skin inflammation by simultaneously enhancing TNF in macrophages and repressing IL-6 in plasmacytoid dendritic cells (pDCs). MCPIP3 is positively associated with psoriasis pathogenesis, and highly expressed by macrophages and pDCs. MCPIP3-deficient macrophages produce less TNF and IL-12p40. However, MCPIP3-deficient pDCs secrete significantly more IL-6. This enhanced intradermal IL-6 may alleviate imiquimod-induced skin inflammation. As a result, MCPIP3-deficient mice are protected from imiquimod-induced psoriasiform lesions. Furthermore, early exposure to pDC-derived IL-6 suppresses macrophage-derived TNF and IL-12p40. Mechanistically, MCPIP3 could directly degrade mRNAs of IL-6, Regnase-1, and IκBζ. In turn, Regnase-1 could degrade MCPIP3 mRNAs. Our study identifies a critical post-transcriptional mechanism that synchronizes myeloid cytokine secretion to initiate autoimmune skin inflammation.
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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 Socratic graph.