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- Title
Association between genetic variation in the gene for death-associated protein-3 (DAP3) and adult asthma.
- Authors
Hirota, Tomomitsu; Obara, Kazuhiko; Matsuda, Akira; Akahoshi, Mitsuteru; Nakashima, Kazuko; Hasegawa, Koichi; Takahashi, Naomi; Shimizu, Makiko; Sekiguchi, Hiroshi; Kokubo, Miki; Doi, Satoru; Fujiwara, Hiroshi; Miyatake, Akihijo; Fujita, Kimie; Enomoto, Tadao; Kishi, Fumio; Suzuki, Yoichi; Saito, Hirohisa; Nakamura, Yusuke; Shirakawa, Taro
- Abstract
Lung epithelium plays a central role in modulation of the lung inflammatory response, and lung repair and airway epithelial cells are targets in asthma and viral infection. Activated T lymphocytes release cytokines such as interferon-gamma (IFN-γ) that induce apoptosis, or programmed cell death, of damaged epithelial cells. Death-associated protein-3 (DAP3) is involved in mediating IFN-γ-induced cell death. To assess the possible involvement of genetic variants of DAP3 with asthma, we searched for single-nucleotide polymorphisms (SNPs) in the gene and conducted a case-control study with 1,341 subjects. We found a strong association between bronchial asthma (BA) in adults (P=0.0051, odds ratio=1.87, 95% CI=1.20–2.92), whereas no association was found with childhood asthma. The tendency was more prominent in patients with higher serum total immunoglobulin E (IgE) (>250 IU/ml) (P=0.00061, odds ratio=2.40, 95% CI=1.44–4.00). DAP3 was expressed in normal bronchial epithelial cells, and the expression was induced by IFN-γ. These results indicated that specific variants of the DAP3 gene might be associated with the mechanisms responsible for adult BA and contribute to airway inflammation and remodeling.
- Subjects
HUMAN genetic variation; PROTEINS; ASTHMA; EPITHELIUM; LYMPHOCYTES; CELL death; NUCLEOTIDES; GENETIC polymorphisms
- Publication
Journal of Human Genetics, 2004, Vol 49, Issue 7, p370
- ISSN
1434-5161
- Publication type
Article
- DOI
10.1007/s10038-004-0161-4