ArticleInternational immunology2016
Innate-like function of memory Th17 cells for enhancing endotoxin-induced acute lung inflammation through IL-22.
Article in International immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Why, Immunologically, Housing-Related Fungi and Endotoxins (and Other Chronic Pro-Inflammatory Stressors) Risk Latent Tuberculosis Reactivation, Severe Asthma, and Translocating and Invasive Infections in Indigenous Communities in Canada.American journal of human biology : the official journal of the Human Biology Council · 2026Review
- An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.The American journal of pathology · 2026Review
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Exploring the pathogenesis of acute lung injury and its treatment through Traditional Chinese Medicine: a state-of-the-art review.Frontiers in pharmacology · 2025Review
- From pancreas to lungs: The role of immune cells in severe acute pancreatitis and acute lung injury.Immunity, inflammation and disease · 2024Review
- Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries.Journal of clinical medicine · 2023Review
- RNA Sequencing Analysis of CD4Critical care explorations · 2023Article
- Macrophage polarization in tissue fibrosis.PeerJ · 2023Review
- Article
- IL-33 Deficiency Attenuates Lung Inflammation by Inducing Th17 Response and Impacting the Th17/Treg Balance in LPS-Induced ARDS Mice via Dendritic Cells.Journal of immunology research · 2022Article
- Dexmedetomidine Activates Akt, STAT6 and IRF4 Modulating Cytoprotection and Macrophage Anti-Inflammatory Phenotype Against Acute Lung Injury in vivo and in vitro.Journal of inflammation research · 2022Article
- Advances in Potential Cerebrospinal Fluid Biomarkers for Autoimmune Encephalitis: A Review.Frontiers in neurology · 2022Review
- Immunotherapy strategies and prospects for acute lung injury: Focus on immune cells and cytokines.Frontiers in pharmacology · 2022Review
- The Role of Th17 Response in COVID-19.Cells · 2021Review
- Resveratrol pretreatment mitigates LPS-induced acute lung injury by regulating conventional dendritic cells' maturation and function.Open life sciences · 2021Article
- Esculetin Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice Via Modulation of the AKT/ERK/NF-κB and RORγt/IL-17 Pathways.Inflammation · 2020Article
- Insights into the immuno-pathogenesis of acute respiratory distress syndrome.Annals of translational medicine · 2019Review
- Effects of Th17 cells and IL-17 in the progression of cervical carcinogenesis with high-risk human papillomavirus infection.Cancer medicine · 2018Article
- Protective Effects of Anti-IL17 on Acute Lung Injury Induced by LPS in Mice.Frontiers in pharmacology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharide (LPS)-induced acute lung injury (ALI) is known as a mouse model of acute respiratory distress syndrome; however, the function of T-cell-derived cytokines in ALI has not yet been established. We found that LPS challenge in one lung resulted in a rapid induction of innate-type pro-inflammatory cytokines such as IL-6 and TNF-α, followed by the expression of T-cell-type cytokines, including IL-17, IL-22 and IFN-γ. We discovered that IL-23 is important for ALI, since blockage of IL-23 by gene disruption or anti-IL-12/23p40 antibody treatment reduced neutrophil infiltration and inflammatory cytokine secretion into the bronchoalveolar lavage fluid (BALF). IL-23 was mostly produced from F4/80(+)CD11c(+) alveolar macrophages, and IL-23 expression was markedly reduced by the pre-treatment of mice with antibiotics, suggesting that the development of IL-23-producing macrophages required commensal bacteria. Unexpectedly, among T-cell-derived cytokines, IL-22 rather than IL-17 or IFN-γ played a major role in LPS-induced ALI. IL-22 protein levels were higher than IL-17 in the BALF after LPS instillation, and the major source of IL-22 was memory Th17 cells. Lung memory CD4(+) T cells had a potential to produce IL-22 at higher levels than IL-17 in response to IL-1β plus IL-23 without TCR stimulation. Our study revealed an innate-like function of the lung memory Th17 cells that produce IL-22 in response to IL-23 and are involved in exaggeration of ALI.
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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.