ArticleInternational immunopharmacology2019
IL-35 interferes with splenic T cells in a clinical and experimental model of acute respiratory distress syndrome.
Article in International immunopharmacology, 2019. 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, 19 citations in OpenAlex.
- The role and mechanism of IL‑35 in myasthenia gravis (Review).International journal of molecular medicine · 2026Review
- Novel therapeutic role of Ganoderma Polysaccharides in a septic mouse model - The key role of macrophages.Heliyon · 2024Article
- Interesting effects of interleukins and immune cells on acute respiratory distress syndrome.Clinical and experimental medicine · 2023Review
- Immunotherapy strategies and prospects for acute lung injury: Focus on immune cells and cytokines.Frontiers in pharmacology · 2022Review
- The Molecular Role of IL-35 in Non-Small Cell Lung Cancer.Frontiers in oncology · 2022Review
- Potential therapeutic effects of interleukin-35 on the differentiation of naïve T cells into HeliosMolecular immunology · 2021Article
- Exploring the metabolic phenotypes associated with different host inflammation of acute respiratory distress syndrome (ARDS) from lung metabolomics in mice.Rapid communications in mass spectrometry : RCM · 2021Article
- Basil Polysaccharide Reverses Development of Experimental Model of Sepsis-Induced Secondary Staphylococcus aureus Pneumonia.Mediators of inflammation · 2021Article
- Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells' maturation and function.Open life sciences · 2021Article
- Coronavirus disease 2019 (COVID-19): cytokine storms, hyper-inflammatory phenotypes, and acute respiratory distress syndrome.Genes & diseases · 2020Review
- Curcumin Promotes the Expression of IL-35 by Regulating Regulatory T Cell Differentiation and Restrains Uncontrolled Inflammation and Lung Injury in Mice.Inflammation · 2020Article
- Pretreatment with interleukin 35-engineered mesenchymal stem cells protected against lipopolysaccharide-induced acute lung injury via pulmonary inflammation suppression.Inflammopharmacology · 2020Article
- Progranulin Improves Acute Lung Injury through Regulating the Differentiation of Regulatory T Cells and Interleukin-10 Immunomodulation to Promote Macrophage Polarization.Mediators of inflammation · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute respiratory distress syndrome (ARDS) is a life-threatening critical care syndrome with uncontrolled inflammation that is a central issue. Its main characteristic is inflammatory mediators and cytokines as well as agglutinating chemokines that injure target cells. Interleukin (IL)-35 is a newly identified IL-12 cytokine family member with structural similarities to other IL-12, IL-23, and IL-27 cytokines but unique immunological functions. How IL-35 functions in ARDS is unclear. The purpose of our study was to determine what role IL-35 played in the development of ARDS. Here we found serum IL-35 concentrations were significantly elevated in patients with ARDS relative to healthy people. Moreover, we established a mouse model of lipopolysaccharide- and cecal ligation and puncture-induced ARDS treated with neutralizing antibodies (anti-IL-35 Ebi3 or anti-IL-35 P35); the results showed that lung injury occurred more often than in untreated models and the inflammatory cytokines CXCL-1, tumor necrosis factor alpha, IL-6, and IL-17A increased significantly after neutralizing antibody treatment in bronchoalveolar lavage fluid and serum. Therefore IL-35 can protect against the development of ARDS. Even more interesting in our study was that we discovered IL-35 expression differed between lung and spleen across different ARDS models, which further demonstrated that the spleen likely has an important role in extrapulmonary ARDS model only, improving the ratio of CD4
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