ArticleThe Journal of clinical investigation2009
CD4+CD25+Foxp3+ Tregs resolve experimental lung injury in mice and are present in humans with acute lung injury.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04482621 (Decitabine for COVID-19 Pneumonia-ARDS Treatment), which is not on this map. Cited by 364 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Decitabine for COVID-19 Pneumonia-ARDS Treatment: DART Trial
Who cites it
364 citing papers in PubMed, 539 citations in OpenAlex.
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- Beyond immune suppression: regenerative programs in regulatory T cells.Cell insight · 2026Review
- Regulatory T Cells in Peri-implant Diseases: Current Osteoimmunologic Perspectives and Translational Challenges.Tissue engineering and regenerative medicine · 2026Review
- T cell receptor signaling induces expression of lysine demethylase KDM6B to maintain Treg homeostasis.The Journal of clinical investigation · 2026Article
- Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Regulatory T cell attracting therapy accelerates skeletal muscle functional recovery following injury.Scientific reports · 2026Article
- CNS1-dependent regulatory T cells shape recovery from acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Understanding the relationship between lung GABABMC pulmonary medicine · 2026Article
- Lung adventitial fibroblasts support type 2 Tregs to shape the response to influenza infection.bioRxiv : the preprint server for biology · 2026Article
- Regulatory T cells protect against aberrant remodeling in a mouse model of pulmonary fibrosis.Mucosal immunology · 2026Article
- Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- CXCL11 levels regulate lung Treg responses to deter the onset of HIV-related COPD.Respiratory research · 2026Article
- Endothelium-Treg Communication Through Extracellular Vesicle Transfer Exacerbates Acute Respiratory Distress Syndrome.Journal of extracellular vesicles · 2026Article
- Alveolar Immune Profiling Identifies Distinct Subphenotypes of Acute Respiratory Failure.medRxiv : the preprint server for health sciences · 2026Article
- Alveolar dysregulation of host response in pneumonia and ARDS: implications for immune modulation and infection.Annals of intensive care · 2026Review
- Single-Cell Insights Into Macrophage Subtypes in Pulmonary Infections.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Induced Regulatory T Cells Attenuate Poly I:C-Triggered Acute Lung Injury by Modulating Cytokine Responses.Journal of immunology research · 2026Article
- Admission CD4Frontiers in cellular and infection microbiology · 2026Observational
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Trends and Prospects in Inflammation Resolution in Acute Lung Injury and Acute Respiratory Distress Syndrome: A Bibliometric Quantitative and Visualization Analysis.Mediators of inflammation · 2026Article
304 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Acute lung injury (ALI) is characterized by rapid alveolar injury, inflammation, cytokine induction, and neutrophil accumulation. Although early events in the pathogenesis of ALI have been defined, the mechanisms underlying resolution are unknown. As a model of ALI, we administered intratracheal (i.t.) LPS to mice and observed peak lung injury 4 days after the challenge, with resolution by day 10. Numbers of alveolar lymphocytes increased as injury resolved. To examine the role of lymphocytes in this response, lymphocyte-deficient Rag-1-/- and C57BL/6 WT mice were exposed to i.t. LPS. The extent of injury was similar between the groups of mice through day 4, but recovery was markedly impaired in the Rag-1-/- mice. Adoptive transfer studies revealed that infusion of CD4+CD25+Foxp3+ Tregs as late as 24 hours after i.t. LPS normalized resolution in Rag-1-/- mice. Similarly, Treg depletion in WT mice delayed recovery. Treg transfer into i.t. LPS-exposed Rag-1-/- mice also corrected the elevated levels of alveolar proinflammatory cytokines and increased the diminished levels of alveolar TGF-beta and neutrophil apoptosis. Mechanistically, Treg-mediated resolution of lung injury was abrogated by TGF-beta inhibition. Moreover, BAL of patients with ALI revealed dynamic changes in CD3+CD4+CD25hiCD127loFoxp3+ cells. These results indicate that Tregs modify innate immune responses during resolution of lung injury and suggest potential targets for treating ALI, for which there are no specific therapies currently available.
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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.