ArticleHuman genetics2009
MICA polymorphisms and decreased expression of the MICA receptor NKG2D contribute to idiopathic pulmonary fibrosis susceptibility.
Article in Human genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- MICA-129Met/Val as a therapeutic compass in idiopathic pulmonary fibrosis: prognosis and antifibrotic benefit.Frontiers in immunology · 2026Article
- Role of telomere dysfunction and immune infiltration in idiopathic pulmonary fibrosis: new insights from bioinformatics analysis.Frontiers in genetics · 2024Article
- Association of MICA Gene Polymorphism in Opisthorchis viverrini-Induced Periductal Fibrosis in Northeastern Thais.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- IL-8 concurrently promotes idiopathic pulmonary fibrosis mesenchymal progenitor cell senescence and PD-L1 expression enabling escape from immune cell surveillance.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- The role of lung-restricted autoantibodies in the development of primary and chronic graft dysfunction.Frontiers in transplantation · 2023Review
- Potential of resveratrol in the treatment of interstitial lung disease.Frontiers in pharmacology · 2023Review
- Recruited and Tissue-Resident Natural Killer Cells in the Lung During Infection and Cancer.Frontiers in immunology · 2022Review
- Blood Transcriptomics Predicts Progression of Pulmonary Fibrosis and Associated Natural Killer Cells.American journal of respiratory and critical care medicine · 2021Article
- Natural killer cells activated through NKG2D mediate lung ischemia-reperfusion injury.The Journal of clinical investigation · 2021Article
- Whole-exome sequencing identifies susceptibility genes and pathways for idiopathic pulmonary fibrosis in the Chinese population.Scientific reports · 2021Article
- Biomarkers for interstitial lung disease and acute-onset diffuse interstitial lung disease in rheumatoid arthritis.Therapeutic advances in musculoskeletal disease · 2021Review
- Integrative Analysis of Transcriptome-Wide Association Study and mRNA Expression Profiles Identifies Candidate Genes Associated With Idiopathic Pulmonary Fibrosis.Frontiers in genetics · 2020Article
- The Influence of Innate Lymphoid Cells and Unconventional T Cells in Chronic Inflammatory Lung Disease.Frontiers in immunology · 2019Review
- NK Cells in the Human Lungs.Frontiers in immunology · 2019Review
- Fine mapping of the major bleomycin-induced pulmonary fibrosis susceptibility locus in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Article
- Role of Microbial Agents in Pulmonary Fibrosis .The Yale journal of biology and medicine · 2017Review
- Genetics in Idiopathic Pulmonary Fibrosis Pathogenesis, Prognosis, and Treatment.Frontiers in medicine · 2017Review
- NK cell activating receptor ligand expression in lymphangioleiomyomatosis is associated with lung function decline.JCI insight · 2016Article
- Genome-wide imputation study identifies novel HLA locus for pulmonary fibrosis and potential role for auto-immunity in fibrotic idiopathic interstitial pneumonia.BMC genetics · 2016Article
- Candidate genes of idiopathic pulmonary fibrosis: current evidence and research.The application of clinical genetics · 2016Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disorder of unknown etiology. IPF is likely the result of complex interrelationships between environmental and host factors, although the genetic risk factors are presently uncertain. Because we have found that some MHC polymorphisms confer susceptibility to IPF, in the present study we aimed to evaluate the role of the MHC class I chain-related gene A (MICA) in the risk of developing the disease. MICA molecular typing was done by reference strand mediated conformation analysis in a cohort of 80 IPF patients and 201 controls. In addition, the lung cellular source of the protein was examined by immunohistochemistry, the expression of the MICA receptor NKG2D in lung cells by flow cytometry and soluble MICA by ELISA. A significant increase of MICA*001 was observed in the IPF cohort (OR = 2.91, 95% CI = 1.04-8.25; pC = 0.03). Likewise, the frequency of the MICA*001/*00201 genotype was significantly increased in patients with IPF compared with the healthy controls (OR = 4.72, 95% CI = 1.15-22.51; pC = 0.01). Strong immunoreactive MICA staining was localized in alveolar epithelial cells and fibroblasts from IPF lungs while control lungs were negative. Soluble MICA was detected in 35% of IPF patients compared with 12% of control subjects (P = 0.0007). The expression of NKG2D was significantly decreased in gammadelta T cells and natural killer cells obtained from IPF lungs. These findings indicate that MICA polymorphisms and abnormal expression of the MICA receptor NKG2D might contribute to IPF susceptibility.
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