Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD
<p>Abstract</p> <p>Background</p> <p>A suggested role for T cells in COPD pathogenesis is based on associations between increased lung cytotoxic T lymphocyte (CD8<sup>+</sup>) numbers and airflow limitation. CD69 is an early T cell activation marker. Natural...
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| Format: | Article |
| Language: | English |
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BMC
2010-09-01
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| Series: | Respiratory Research |
| Online Access: | http://respiratory-research.com/content/11/1/128 |
| _version_ | 1811267014022397952 |
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| author | Behndig Annelie F Pourazar Jamshid Roos-Engstrand Ester Blomberg Anders Bucht Anders |
| author_facet | Behndig Annelie F Pourazar Jamshid Roos-Engstrand Ester Blomberg Anders Bucht Anders |
| author_sort | Behndig Annelie F |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>A suggested role for T cells in COPD pathogenesis is based on associations between increased lung cytotoxic T lymphocyte (CD8<sup>+</sup>) numbers and airflow limitation. CD69 is an early T cell activation marker. Natural Killer cell group 2 D (NKG2D) receptors are co-stimulatory molecules induced on CD8<sup>+ </sup>T cells upon activation. The activating function of NKG2 D is triggered by binding to MHC class 1 chain-related (MIC) molecules A and B, expressed on surface of stressed epithelial cells. The aim of this study was to evaluate the expression of MIC A and B in the bronchial epithelium and NKG2 D and CD69 on BAL lymphocytes in subjects with COPD, compared to smokers with normal lung function and healthy never-smokers.</p> <p>Methods</p> <p>Bronchoscopy with airway lavages and endobronchial mucosal biopsy sampling was performed in 35 patients with COPD, 21 healthy never-smokers and 16 smokers with normal lung function. Biopsies were immunohistochemically stained and BAL lymphocyte subsets were determined using flow cytometry.</p> <p>Results</p> <p>Epithelial CD3<sup>+ </sup>lymphocytes in bronchial biopsies were increased in both smokers with normal lung function and in COPD patients, compared to never-smokers. Epithelial CD8<sup>+ </sup>lymphocyte numbers were higher in the COPD group compared to never-smoking controls. Among gated CD3<sup>+</sup>cells in BAL, the percentage of CD8<sup>+ </sup>NKG2D<sup>+ </sup>cells was enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. The percentage of CD8<sup>+ </sup>CD69<sup>+ </sup>cells and cell surface expression of CD69 were enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. No changes in the expression of MIC A or MIC B in the airway epithelium could be detected between the groups, whereas significantly decreased soluble MICB was detected in bronchial wash from smokers with normal lung function, compared to never-smokers.</p> <p>Conclusions</p> <p>In COPD, we found increased numbers of cytotoxic T cells in both bronchial epithelium and airway lumen. Further, the proportions of CD69- and NKG2D-expressing cytotoxic T cells in BAL fluid were enhanced in both subjects with COPD and smokers with normal lung function and increased expression of CD69 was found on CD8<sup>+ </sup>cells, indicating the cigarette smoke exposure-induced expansion of activated cytotoxic T cells, which potentially can respond to stressed epithelial cells.</p> |
| first_indexed | 2024-04-12T20:53:38Z |
| format | Article |
| id | doaj.art-9107b2d05ef443c288a1c5e8a28d940a |
| institution | Directory Open Access Journal |
| issn | 1465-9921 |
| language | English |
| last_indexed | 2024-04-12T20:53:38Z |
| publishDate | 2010-09-01 |
| publisher | BMC |
| record_format | Article |
| series | Respiratory Research |
| spelling | doaj.art-9107b2d05ef443c288a1c5e8a28d940a2022-12-22T03:17:02ZengBMCRespiratory Research1465-99212010-09-0111112810.1186/1465-9921-11-128Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPDBehndig Annelie FPourazar JamshidRoos-Engstrand EsterBlomberg AndersBucht Anders<p>Abstract</p> <p>Background</p> <p>A suggested role for T cells in COPD pathogenesis is based on associations between increased lung cytotoxic T lymphocyte (CD8<sup>+</sup>) numbers and airflow limitation. CD69 is an early T cell activation marker. Natural Killer cell group 2 D (NKG2D) receptors are co-stimulatory molecules induced on CD8<sup>+ </sup>T cells upon activation. The activating function of NKG2 D is triggered by binding to MHC class 1 chain-related (MIC) molecules A and B, expressed on surface of stressed epithelial cells. The aim of this study was to evaluate the expression of MIC A and B in the bronchial epithelium and NKG2 D and CD69 on BAL lymphocytes in subjects with COPD, compared to smokers with normal lung function and healthy never-smokers.</p> <p>Methods</p> <p>Bronchoscopy with airway lavages and endobronchial mucosal biopsy sampling was performed in 35 patients with COPD, 21 healthy never-smokers and 16 smokers with normal lung function. Biopsies were immunohistochemically stained and BAL lymphocyte subsets were determined using flow cytometry.</p> <p>Results</p> <p>Epithelial CD3<sup>+ </sup>lymphocytes in bronchial biopsies were increased in both smokers with normal lung function and in COPD patients, compared to never-smokers. Epithelial CD8<sup>+ </sup>lymphocyte numbers were higher in the COPD group compared to never-smoking controls. Among gated CD3<sup>+</sup>cells in BAL, the percentage of CD8<sup>+ </sup>NKG2D<sup>+ </sup>cells was enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. The percentage of CD8<sup>+ </sup>CD69<sup>+ </sup>cells and cell surface expression of CD69 were enhanced in patients with COPD and smokers with normal lung function, compared to never-smokers. No changes in the expression of MIC A or MIC B in the airway epithelium could be detected between the groups, whereas significantly decreased soluble MICB was detected in bronchial wash from smokers with normal lung function, compared to never-smokers.</p> <p>Conclusions</p> <p>In COPD, we found increased numbers of cytotoxic T cells in both bronchial epithelium and airway lumen. Further, the proportions of CD69- and NKG2D-expressing cytotoxic T cells in BAL fluid were enhanced in both subjects with COPD and smokers with normal lung function and increased expression of CD69 was found on CD8<sup>+ </sup>cells, indicating the cigarette smoke exposure-induced expansion of activated cytotoxic T cells, which potentially can respond to stressed epithelial cells.</p>http://respiratory-research.com/content/11/1/128 |
| spellingShingle | Behndig Annelie F Pourazar Jamshid Roos-Engstrand Ester Blomberg Anders Bucht Anders Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD Respiratory Research |
| title | Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD |
| title_full | Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD |
| title_fullStr | Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD |
| title_full_unstemmed | Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD |
| title_short | Cytotoxic T cells expressing the co-stimulatory receptor NKG2 D are increased in cigarette smoking and COPD |
| title_sort | cytotoxic t cells expressing the co stimulatory receptor nkg2 d are increased in cigarette smoking and copd |
| url | http://respiratory-research.com/content/11/1/128 |
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