ArticleNature communications2017
IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.
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Who cites it
140 citing papers in PubMed, 225 citations in OpenAlex.
- Sepsis subtypes and differential treatment response to vitamin C: biological sub-study of the LOVIT trial.Intensive care medicine · 2025Trial
- Targeting the NR1D1-IGF2BP2-V-ATPase Axis With Hybrid Nanovesicles Restores Macrophage Rhythms to Reverse Sepsis-Induced Immunosuppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sepsis-related immunosuppression: a comprehensive review of current research breakthroughs.Critical care (London, England) · 2026Review
- HMGB1-mediated formation of IL-33-abundant NETs drives lung-to-kidney injury in severe pneumonia-associated acute kidney injury.JCI insight · 2026Article
- Review
- Article
- Ion interference induced by Ca-Mn nanoplatform enhances ferroptosis and promotes immune response for osteosarcoma treatment.Journal of advanced research · 2026Article
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- Single-Cell and Spatial Transcriptomics Identify the Mono-S100A4 Subset Associated with Sepsis-Induced Lung Injury via the MIF-(CD74+CD44) Axis.Journal of inflammation research · 2026Article
- Prognostic Value of SIRS, SOFA, qSOFA, and LqSOFA in Emergency Department Sepsis Patients and Correlation of Cytokine Patterns With In-Hospital Mortality.Journal of clinical medicine research · 2025Article
- IL-1 family cytokines in inflammation and immunity.Cellular & molecular immunology · 2025Review
- The Multifaceted Role of Regulatory T Cells in Sepsis: Mechanisms, Heterogeneity, and Pathogen-Tailored Therapies.International journal of molecular sciences · 2025Review
- The Role of Eosinophils, Eosinophil-Related Cytokines and AI in Predicting Immunotherapy Efficacy in NSCLCBiomolecules · 2025Review
- The Impact of Steatotic Liver Disease on Cytokine and Chemokine Kinetics During Sepsis.International journal of molecular sciences · 2025Article
- Group 2 innate lymphoid cells derived IL-9 reduces macrophage apoptosis and attenuates acute lung injury in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Dysregulated Immune Responses in Sepsis: Insights From Treg-Related Gene Expression.Journal of inflammation research · 2025Article
- The homeostasis and heterogeneity of regulatory T cells in sepsis.Burns & trauma · 2025Article
- Sepsis-induced immunosuppression: mechanisms, biomarkers and immunotherapy.Frontiers in immunology · 2025Review
- Considering local immunity for innovative immunomodulatory approaches: pulmonary sepsis as a use case.Frontiers in immunology · 2025Review
- Cell-cell crosstalk in the pathogenesis of acute lung injury and acute respiratory distress syndrome.Tissue barriers · 2025Review
80 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients who survive sepsis can develop long-term immune dysfunction, with expansion of the regulatory T (Treg) cell population. However, how Treg cells proliferate in these patients is not clear. Here we show that IL-33 has a major function in the induction of this immunosuppression. Mice deficient in ST2 (IL-33R) develop attenuated immunosuppression in cases that survive sepsis, whereas treatment of naive wild-type mice with IL-33 induces immunosuppression. IL-33, released during tissue injury in sepsis, activates type 2 innate lymphoid cells, which promote polarization of M2 macrophages, thereby enhancing expansion of the Treg cell population via IL-10. Moreover, sepsis-surviving patients have more Treg cells, IL-33 and IL-10 in their peripheral blood. Our study suggests that targeting IL-33 may be an effective treatment for sepsis-induced immunosuppression.
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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.