| Downregulation of integrin β4 decreases the ability of airway epithelial cells to present antigens. | |
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MedLine Citation:
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PMID: 22545078 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Airway epithelial cells have been demonstrated to be accessory antigen presentation cells (APC) capable of activating T cells and may play an important role in the development of allergic airway inflammation of asthma. In asthmatic airways, loss of expression of the adhesion molecule integrin β4 (ITGB4) and an increase in Th2 inflammation bias has been observed in our previous study. Given that ITGB4 is engaged in multiple signaling pathways, we studied whether disruption of ITGB4-mediated cell adhesion may contribute to the adaptive immune response of epithelial cells, including their ability to present antigens, induce the activate and differentiate of T cells. We silenced ITGB4 expression in bronchial epithelial cells with an effective siRNA vector and studied the effects of ITGB4 silencing on the antigen presentation ability of airway epithelial cells. T cell proliferation and cytokine production was investigated after co-culturing with ITGB4-silenced epithelial cells. Surface expression of B7 homologs and the major histocompatibility complex (MHC) class II was also detected after ITGB4 was silenced. Our results demonstrated that silencing of ITGB4 resulted in impaired antigen presentation processes and suppressed T cell proliferation. Meanwhile, decrease in Th1 cytokine production and increase in Th17 cytokine production was induced after co-culturing with ITGB4-silenced epithelial cells. Moreover, HLA-DR was decreased and the B7 homologs expression was different after ITGB4 silencing. Overall, this study suggested that downregulation of ITGB4 expression in airway epithelial cells could impair the antigen presentation ability of these cells, which further regulate airway inflammation reaction in allergic asthma. |
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Authors:
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Chi Liu; Xiaoqun Qin; Huijun Liu; Yang Xiang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2012-04-24 |
Journal Detail:
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Title: PloS one Volume: 7 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2012 |
Date Detail:
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Created Date: 2012-04-30 Completed Date: 2012-08-27 Revised Date: 2013-05-20 |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e32060 Citation Subset: IM |
Affiliation:
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Physiology Department, Xiangya Medical School, Central South University, Changsha, Hunan, People's Republic of China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigen Presentation* Asthma / genetics, immunology Bronchi / cytology Cell Adhesion Cell Line Cell Proliferation Cytokines / immunology Down-Regulation* Epithelial Cells / immunology*, metabolism HLA-DR Antigens / analysis, immunology Humans Integrin beta4 / genetics*, immunology* Lymphocyte Activation RNA Interference RNA, Small Interfering / genetics Respiratory Mucosa / cytology, immunology*, metabolism T-Lymphocytes / cytology, immunology* |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/HLA-DR Antigens; 0/Integrin beta4; 0/RNA, Small Interfering |
| Comments/Corrections | |
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