ArticleJCI insight2020
Regnase-1 degradation is crucial for IL-33- and IL-25-mediated ILC2 activation.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- The regnase family in autoimmune diseases: a regnase-1-centered perspective on cellular heterogeneity.Molecular biology reports · 2026Review
- Decoding Regnase-1's role in skin inflammation: potential therapeutic implication for dermatological disorders.Journal of advanced research · 2026Review
- Fungal exposure exacerbates allergen-driven asthma in a two-hit mouse model.Respiratory research · 2026Article
- The Regnase pathway: a core axis in immune regulation and inflammatory disease.Frontiers in immunology · 2026Review
- The RNA-Binding Protein KSRP Is a Negative Regulator of Innate Immunity.Biomolecules · 2025Review
- Molecular mechanisms regulating T helper 2 cell differentiation and function.Current opinion in immunology · 2024Review
- Crosstalk between Regnase-1 and -3 shapes mast cell survival and cytokine expression.Life science alliance · 2024Article
- Mef2d potentiates type-2 immune responses and allergic lung inflammation.Science (New York, N.Y.) · 2024Article
- Blocking group 2 innate lymphoid cell activation and macrophage M2 polarization: potential therapeutic mechanisms in ovalbumin-induced allergic asthma by calycosin.BMC pharmacology & toxicology · 2024Article
- RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024Review
- Time-dependent cell-state selection identifies transiently expressed genes regulating ILC2 activation.Communications biology · 2023Article
- The immunomodulatory role of Regnase family RNA-binding proteins.RNA biology · 2020Review
- MCPIP1 RNase and Its Multifaceted Role.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2s) are a critical innate source of type 2 cytokines in allergic inflammation. Although ILC2s are recognized as a critical cell population in the allergic inflammation, the regulatory mechanism(s) of ILC2s are less well understood. Here, we show that Regnase-1, an immune regulatory RNAse that degrades inflammatory mRNAs, negatively regulates ILC2 function and that IκB kinase (IKK) complex-mediated Regnase-1 degradation is essential for IL-33- and IL-25-induced ILC2 activation. ILC2s from Regnase-1AA/AA mice expressing a Regnase-1 S435A/S439A mutant resistant to IKK complex-mediated degradation accumulated Regnase-1 protein in response to IL-33 and IL-25. IL-33- and IL-25-stimulated Regnase-1AA/AA ILC2s showed reduced cell proliferation and type 2 cytokine (IL-5, IL-9, and IL-13) production and increased cell death. In addition, Il2ra and Il1rl1, but not Il5, Il9, or Il13, mRNAs were destabilized in IL-33-stimulated Regnase-1AA/AA ILC2s. In vivo, Regnase-1AA/AA mice showed attenuated acute type 2 pulmonary inflammation induced by the instillation of IL-33, IL-25, or papain. Furthermore, the expulsion of Nippostrongylus brasiliensis was significantly delayed in Regnase-1AA/AA mice. These results demonstrate that IKK complex-mediated Regnase-1 degradation is essential for ILC2-mediated type 2 responses both in vitro and in vivo. Therefore, controlling Regnase-1 degradation is a potential therapeutic target for ILC2-contributed allergic disorders.
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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.