ArticleThe American journal of pathology2012
Cytokine-like factor 1 gene expression is enriched in idiopathic pulmonary fibrosis and drives the accumulation of CD4+ T cells in murine lungs: evidence for an antifibrotic role in bleomycin injury.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Blood gene expression risk profiles and interstitial lung abnormalities: COPDGene and ECLIPSE cohort studies.Respiratory research · 2022Pooled it
- Lung disease in crisponi/cold-induced sweating syndrome type 1: expanding the clinical phenotype spectrum.European journal of pediatrics · 2026Article
- Cardiotrophin-like cytokine factor 1 forms a complex with IL12/IL23p40.Scientific reports · 2025Article
- Spatial transcriptomics defines injury specific microenvironments and cellular interactions in kidney regeneration and disease.Nature communications · 2024Article
- Cellular and Molecular Genetic Mechanisms of Lung Fibrosis Development and the Role of Vitamin D: A Review.International journal of molecular sciences · 2024Review
- Detection of CLCF1 protein expression by flow cytometry.Scientific reports · 2024Article
- Spatial transcriptomics defines injury-specific microenvironments in the adult mouse kidney and novel cellular interactions in regeneration and disease.bioRxiv : the preprint server for biology · 2023Article
- Pulmonary inflammation and fibroblast immunoregulation: from bench to bedside.The Journal of clinical investigation · 2023Review
- Role of Interleukin-6 Family Cytokines in Organ Fibrosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Exploration of the shared genes and signaling pathways between lung adenocarcinoma and idiopathic pulmonary fibrosis.Journal of thoracic disease · 2023Article
- T cells in idiopathic pulmonary fibrosis: crucial but controversial.Cell death discovery · 2023Review
- Identification of diagnostic hub genes related to neutrophils and infiltrating immune cell alterations in idiopathic pulmonary fibrosis.Frontiers in immunology · 2023Article
- CRLF1 and CLCF1 in Development, Health and Disease.International journal of molecular sciences · 2022Review
- The Role of Interleukin-6 Family Members in Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Review
- Transcriptomic Mapping of Non-Small Cell Lung CancerFrontiers in immunology · 2021Article
- Akt1 regulates pulmonary fibrosis via modulating IL-13 expression in macrophages.Innate immunity · 2019Article
- Fine mapping of the major bleomycin-induced pulmonary fibrosis susceptibility locus in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Activated human T lymphocytes inhibit TGFβ-induced fibroblast to myofibroblast differentiation via prostaglandins DAmerican journal of physiology. Lung cellular and molecular physiology · 2018Article
- Impact of Transcriptomics on Our Understanding of Pulmonary Fibrosis.Frontiers in medicine · 2018Review
- Loss of Twist1 in the Mesenchymal Compartment Promotes Increased Fibrosis in Experimental Lung Injury by Enhanced Expression of CXCL12.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and typically fatal lung disease. To gain insight into the pathogenesis of IPF, we reanalyzed our previously published gene expression data profiling IPF lungs. Cytokine receptor-like factor 1 (CRLF1) was among the most highly up-regulated genes in IPF lungs, compared with normal controls. The protein product (CLF-1) and its partner, cardiotrophin-like cytokine (CLC), function as members of the interleukin 6 (IL-6) family of cytokines. Because of earlier work implicating IL-6 family members in IPF pathogenesis, we tested whether CLF-1 expression contributes to inflammation in experimental pulmonary fibrosis. In IPF, we detected CLF-1 expression in both type II alveolar epithelial cells and macrophages. We found that the receptor for CLF-1/CLC signaling, ciliary neurotrophic factor receptor (CNTFR), was expressed only in type II alveolar epithelial cells. Administration of CLF-1/CLC to both uninjured and bleomycin-injured mice led to the pulmonary accumulation of CD4(+) T cells. We also found that CLF-1/CLC administration increased inflammation but decreased pulmonary fibrosis. CLF-1/CLC leads to significantly enriched expression of T-cell-derived chemokines and cytokines, including the antifibrotic cytokine interferon-γ. We propose that, in IPF, CLF-1 is a selective stimulus of type II alveolar epithelial cells and may potentially drive an antifibrotic response by augmenting both T-helper-1-driven and T-regulatory-cell-driven inflammatory responses in the lung.
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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.