ArticleThe Journal of biological chemistry2013
The serine-threonine kinase inositol-requiring enzyme 1α (IRE1α) promotes IL-4 production in T helper cells.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- Metabolic and stress response adaptations in T cells to fever and physiological heat.Trends in immunology · 2025Review
- Pharmacological Modulation of the Unfolded Protein Response as a Therapeutic Approach in Cutaneous T-Cell Lymphoma.Biomolecules · 2025Article
- TMED4 facilitates regulatory T cell suppressive function via ROS homeostasis in tumor and autoimmune mouse models.The Journal of clinical investigation · 2024Article
- IRE1α pathway: A potential bone metabolism mediator.Cell proliferation · 2024Review
- Emerging mechanisms of the unfolded protein response in therapeutic resistance: from chemotherapy to Immunotherapy.Cell communication and signaling : CCS · 2024Review
- Navigating the landscape of the unfolded protein response in CD8Frontiers in immunology · 2024Review
- Exploiting autophagy balance in T and NK cells as a new strategy to implement adoptive cell therapies.Molecular cancer · 2023Review
- Essential requirement for IER3IP1 in B cell development.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Proteostasis in T cell aging.Seminars in immunology · 2023Review
- Beyond UPR: cell-specific roles of ER stress sensor IRE1α in kidney ischemic injury and transplant rejection.Kidney international · 2023Review
- Article
- IRE1α arm of unfolded protein response in muscle-specific TGF-β signaling-mediated regulation of muscle cell immunological properties.Cellular & molecular biology letters · 2023Article
- Asthmatic lung fibroblasts promote type 2 immune responsesFrontiers in physiology · 2023Article
- Sensor dimer disruption as a new mode of action to block the IRE1-mediated unfolded protein response.Computational and structural biotechnology journal · 2022Article
- XBP1 is required in Th2 polarization induction in airway allergy.Theranostics · 2022Article
- Endoplasmic Reticulum Quality Control in Immune Cells.Frontiers in cell and developmental biology · 2021Review
- Induction of the Unfolded Protein Response during Bovine Alphaherpesvirus 1 Infection.Viruses · 2020Article
- Endoplasmic reticulum-associated degradation and beyond: The multitasking roles for HRD1 in immune regulation and autoimmunity.Journal of autoimmunity · 2020Review
- ORMDL3 and Asthma: Linking Sphingolipid Regulation to Altered T Cell Function.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The inositol-requiring enzyme 1α (IRE1α) is a serine-threonine kinase that plays crucial roles in activating the unfolded protein response. Studies suggest that IRE1α is activated during thymic T cell development and in effector CD8(+) T cells. However, its role in regulating T helper cell differentiation remains unknown. We find that IRE1α is up-regulated and activated upon CD4(+) T cell activation and plays an important role in promoting cytokine IL-4 production. CD4(+) T cells from IRE1α KO mice have reduced IL-4 protein expression, and this impaired IL-4 production is not due to the altered expression of Th2 lineage-specific transcription factors, such as GATA3. Instead, IL-4 mRNA stability is reduced in IRE1α KO T cells. Furthermore, treatment of T cells with an IRE1α-specific inhibitor, 4μ8C, leads to a block in IL-4, IL-5, and IL-13 production, confirming the role of IRE1α in the regulation of IL-4. This study identifies a regulatory function for IRE1α in the promotion of IL-4 in T cells.
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Registered trials
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.