A comparison of the expression of lymphocyte activation markers in blood, bronchial biopsies and bronchoalveolar lavage: evidence for an enrichment of activated T lymphocytes in the bronchoalveolar space

Ekberg-Jansson, Ann; Arvå, E; Nilsson, Ola; Löfdahl, Claes-Göran; Åndersson, Bengt

doi:10.1016/s0954-6111(99)90156-7

Cited by 20 publications

(21 citation statements)

References 18 publications

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“…Secondly, no significant differences were found between groups in any of the different markers studied in peripheral blood, whereas marked compartmentalisation was observed when blood and BALF samples were compared (tables 3 and 4). These observations agree with previous studies [29][30][31] and suggest that differences observed in BALF (previously discussed) are due to specific recruitment and/or local activation in the lungs.…”

Section: Cd25 Treg Cells In Copd B Barceló Et Alsupporting

confidence: 93%

Phenotypic characterisation of T-lymphocytes in COPD: abnormal CD4+CD25+ regulatory T-lymphocyte response to tobacco smoking

Barceló¹,

Pons²,

Ferrer³

et al. 2008

European Respiratory Journal

169

124

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Tobacco smoking induces an inflammatory response in the lungs of all smokers but, for reasons that are still poorly understood, only a proportion of them develop chronic obstructive pulmonary disease (COPD). Recent evidence indicates that this inflammatory response persists after smoking cessation, suggesting some type of auto-perpetuation mechanism similar to that described in autoimmune disorders. T-lymphocytes (CD4+ and CD8+) have been implicated in the pathogenesis of both COPD and several autoimmune processes. A subtype of regulatory CD4+ T-cells expressing CD25 (Tregs) plays a critical role in the maintenance of peripheral tolerance and the prevention of autoimmunity, but their potential role in COPD has not been explored. The present study sought to evaluate maturation (CD45RA/CD45R0) and activation markers (CD28) of T-lymphocytes and to explore potential Treg abnormalities in COPD.Flow cytometry was used to characterise T-lymphocytes obtained from blood and bronchoalveolar lavage fluid (BALF) in 23 patients with moderate COPD, 29 smokers with normal lung function and seven never-smokers.The main findings were that in BALF: patients with COPD showed higher CD8+CD45RA+ and lower CD8+CD45R0+ than smokers with normal lung function; and compared with never-smokers, smokers with preserved lung function showed a prominent upregulation of Tregs that was absent in patients with COPD.These observations indicate a final maturation-activation state of CD8+ T-lymphocytes in chronic obstructive pulmonary disease and, for the first time, identify a blunted regulatory T-cell response to tobacco smoking in these patients, further supporting a potential involvement of the acquired immune response in the pathogenesis of the disease.

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Section: Cd25 Treg Cells In Copd B Barceló Et Alsupporting

confidence: 93%

Phenotypic characterisation of T-lymphocytes in COPD: abnormal CD4+CD25+ regulatory T-lymphocyte response to tobacco smoking

Barceló¹,

Pons²,

Ferrer³

et al. 2008

European Respiratory Journal

169

124

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“…Normal BAL fluid is characterized by a proportion of lymphocytes of 5-15% (22), which includes activated (23,24) and granzyme B geneexpressing (14) lymphocytes. The presence of such activated alveolar lymphocytes in the normal setting could explain the presence of low levels of granzymes in some healthy subjects.…”

Section: Discussionmentioning

confidence: 99%

Granzyme Activity in the Inflamed Lung Is Not Controlled by Endogenous Serine Proteinase Inhibitors

Tremblay

Wolbink

Cormier

et al. 2000

The Journal of Immunology

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Numerous lung diseases, such as hypersensitivity pneumonitis (HP), are characterized by the presence of activated alveolar CTL and NK cells. Since these cells produce granzymes, granzyme A and B levels in bronchoalveolar lavage (BAL) fluids from 14 normal subjects and 12 patients with HP were measured by ELISA. Median (range) BAL granzyme A and B levels were 4 (0–37) and 0 (0–6) pg/ml in normal subjects. BAL granzyme levels were significantly higher in HP patients, being at 74 (0–1889) and 10 (0–78) pg/ml for granzymes A and B, respectively. In vitro, neither of the three main serine protease inhibitors of the lung, namely α1-antitrypsin, secretory leukocyte protease inhibitor, and elafin, showed any effect on granzyme A or B activity. In addition, granzyme A was shown to be fully active in BAL fluids. Hence, these data show that granzyme activity may be poorly controlled by protease inhibitors in inflamed tissues. Thus, granzymes could contribute to tissue remodeling and inflammation characterizing HP.

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confidence: 99%

“…A substantial number of other co-stimulatory molecules and their ligands have been identified in recent years [12]. EKBERG-JANSSON et al [12] reported a greater proportion of T-lymphocyte activation markers (human leukocyte antigen (HLA)-DR, CD26+, CD54+, CD69+) in bronchoalveolar lavage (BAL) fluid compared with blood in nonsmokers. Moreover, GLADER et al [7] showed a clear correlation between expression of the activation marker CD69 on CD4+ T-cells and lung function (forced expiratory volume in one second (FEV1)) in current smokers with and without COPD, indicating smoking-induced impairment of T-cell activation.…”

mentioning

confidence: 99%

Modification of surface antigens in blood CD8+ T-lymphocytes in COPD: effects of smoking

Koch¹,

Gaczkowski²,

Sturton³

et al. 2006

European Respiratory Journal

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In contrast to the effects of cigarette smoke on T-lymphocyte subsets in the airways, it has not yet been determined whether smoking has immunomodulatory effects on surface antigens of peripheral blood T-lymphocytes and, if that is the case, whether these effects differ in smokers with and without chronic obstructive pulmonary disease (COPD).The present authors have, therefore, examined the expression of the surface activation marker CD28, the levels of cytotoxic effector lymphocytes (CD27-/CD45RA+) and the expression of the lung type (Tc)1-specific chemokine receptor CXCR 3 + on peripheral blood CD8+ T-lymphocytes. The present authors have also studied the chemotactic activity of CD8+ T-lymphocytes on monocyte chemotactic protein (MCP)-1 and compared 13 nonsmoking controls, 12 smokers with COPD and 14 smokers without airflow limitation.There was a decrease in the total count of CD8+ T-cells and an increase in the CD4+/CD8+ ratio in smokers with COPD compared with smokers without COPD and controls. Expression of the Tc1-specific chemokine receptor CXCR 3 + by CD8+ T-cells was increased in smokers with COPD compared with smokers without COPD and controls.The expression of activated and of cytotoxic effector CD8+ T-cells in smokers with and without COPD showed an increase compared with controls. CD8+ T-cells from smokers with and without COPD showed a decrease in chemotactic activity to MCP-1 compared with controls.In conclusion, chronic obstructive pulmonary disease may be a systemic immunomodulatory disease associated with the modification of surface antigens in blood CD8+ T-lymphocytes.

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A comparison of the expression of lymphocyte activation markers in blood, bronchial biopsies and bronchoalveolar lavage: evidence for an enrichment of activated T lymphocytes in the bronchoalveolar space

Cited by 20 publications

References 18 publications

Phenotypic characterisation of T-lymphocytes in COPD: abnormal CD4+CD25+ regulatory T-lymphocyte response to tobacco smoking

Phenotypic characterisation of T-lymphocytes in COPD: abnormal CD4+CD25+ regulatory T-lymphocyte response to tobacco smoking

Granzyme Activity in the Inflamed Lung Is Not Controlled by Endogenous Serine Proteinase Inhibitors

Modification of surface antigens in blood CD8+ T-lymphocytes in COPD: effects of smoking

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