ArticleThe Journal of experimental medicine2010
γδ T cells protect against lung fibrosis via IL-22.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
142 citing papers in PubMed, 232 citations in OpenAlex.
- Extracellular RNA clearance by non-canonical cell-surface MDA5 protects against lung fibrosis.EMBO molecular medicine · 2026Article
- Collaborative functionality between three types of inflammation in idiopathic pulmonary fibrosis.Nature immunology · 2026Review
- How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- The effects of physical exercise on inflammation-induced maladaptive neuroplasticity in post-traumatic headache.Neuroscience · 2026Review
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Tweaking the Complex Fibrogenic Role of Lymphocytes in Idiopathic Pulmonary Fibrosis.Tuberculosis and respiratory diseases · 2026Article
- An Update on IL-22 Therapies in Alcohol-Associated Liver Disease and Beyond.The American journal of pathology · 2026Review
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Intestinal Fibrosis in Crohn's Disease: Pathophysiology, Diagnosis, and New Therapeutic Targets.Journal of clinical medicine · 2025Review
- Sex-dependent modulation of acute respiratory distress syndrome byFrontiers in immunology · 2025Article
- The role of aryl hydrocarbon receptor signalling in COVID-19 pathology and its therapeutic potential.Frontiers in molecular medicine · 2025Review
- Review
- IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024Review
- IL-22 Binding Protein Controls IL-22-Driven Bleomycin-Induced Lung Injury.The American journal of pathology · 2024Article
- Interplay between Microbiota and γδ T Cells: Insights into Immune Homeostasis and Neuro-Immune Interactions.International journal of molecular sciences · 2024Review
- Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3Frontiers in immunology · 2024Article
- Hub genes identification and validation of ferroptosis in SARS-CoV-2 induced ARDS: perspective from transcriptome analysis.Frontiers in immunology · 2024Article
- A single-cell atlas of the aging mouse ovary.Nature aging · 2024Article
- The Role of Immune Cells in the Pathogenesis of Idiopathic Pulmonary Fibrosis.Medicina (Kaunas, Lithuania) · 2023Review
- Double-edged sword: γδ T cells in mucosal homeostasis and disease.Experimental & molecular medicine · 2023Review
82 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammation-induced pulmonary fibrosis (PF) leads to irreversible loss of lung function and is a predictor of mortality in numerous lung diseases. Why some subjects with lung inflammation but not others develop PF is unclear. In a mouse model of hypersensitivity pneumonitis that progresses to lung fibrosis upon repeated exposure to the ubiquitous microorganism Bacillus subtilis, γδ T cells expand in the lung and inhibit collagen deposition. We show that a subset of these γδ cells represents the predominant source of the Th17 cytokine IL-22 in this model. Preventing expression of IL-22, either by mutating the aryl hydrocarbon receptor (AhR) or inhibiting AhR signaling, accelerated lung fibrosis. Direct blockade of IL-22 also enhanced collagen deposition in the lung, whereas administration of recombinant IL-22 inhibited lung fibrosis. Moreover, the presence of protective γδ T cells and IL-22 diminished recruitment of CD4(+) T cells to lung. These data reveal a protective pathway that involves the inhibition of αβ T cells by regulatory IL-22-secreting γδ T cells.
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What OpenQuestion holds
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.