The aim of this study was to explore the presence of interleukin (IL)-16 in pleural effusions, the correlation between IL-16 levels and cytological parameters, as well as the chemoattractant activity of IL-16 on CD4+ T-lymphocytes. Total nucleated cell and differential counts, and IL-16 concentrations in the pleural effusion from 32 patients with tuberculous pleurisy and 30 patients with lung cancer were determined. Threecolour flow cytometry was performed to determine T-lymphocyte subsets in cell pellets of pleural effusion. The chemoattractant activity of IL-16 for CD4+ T-lymphocytes was also analysed. The levels of IL-16 were significantly higher in tuberculous than in malignant effusions. However, IL-16 levels could not be used for diagnostic purposes due to significant overlap between the two groups. Positive correlations were found between the IL-16 levels and CD4+ Tcells, and pleural fluid was chemotactic for CD4+ T-cells in vitro. Intrapleural administration of IL-16 to patients produced a marked progressive influx of CD4+ T-cells into the pleural space. Compared with malignant pleural effusion, interleukin-16 appeared to be increased in tuberculous pleural effusion. Interleukin-16 levels were positively related to the numbers of CD4+ T-cells, and interleukin-16 could directly induce CD4+ T-cell infiltration into the pleuralspace.

Cytotoxic lymphocyte associated antigen-4 (CTLA-4) is a homologue of CD28, which plays a critical role in the down-regulation of antigenactivated immune response. The aim of the present study was to investigate the concentrations of soluble CTLA-4 in sera of patients with bronchial asthma and the correlation between soluble CTLA-4 concentrations and some clinical measures of asthma. The concentrations of serum soluble CTLA-4 in 31 atopic asthmatics, 20 non-atopic asthmatics, and 28 non-atopic normal control volunteers were determined by ELISA technique, and the relationship between serum soluble CTLA-4 concentrations in asthmatics and airway responsiveness, pulmonary function, blood white cell counts and differentials, respectively, were analyzed. Serum soluble CTLA-4 concentrations in both atopic asthmatics (20.2

The aim of the present study was to investigate effects of allergen inhalation and oral glucocorticoid on concentration of serum soluble CD86 in patients with allergic asthma. Our results showed that the serum soluble CD86 concentrations in the dual responder group increased from 491.8 F 15.4 IU/ml before allergen inhalation to 603.8 F 19.3 IU/ml 24 h after allergen inhalation. In the isolated early responders, there was no significant increase in serum soluble CD86 concentrations after allergen inhalation compared with baseline levels. There was a significant decrease in serum soluble CD86 concentrations after 2 weeks of glucocorticoid therapy (448.3 F 15.1 IU/ml) compared with baseline values (532.7 F 12.3 IU/ml), whereas there was no significant difference in the placebo group. This study has demonstrated that serum soluble CD86 concentrations increased after allergen inhalation in sensitized asthmatic subjects, and that serum sCD86 concentrations were downregulated by prednisolone therapy.

Background: Previous studies have reported that soluble (s) CD86 is involved in the initiation of the immune response. A study was undertaken to investigate the concentrations of sCD86 in serum samples from patients with bronchial asthma and to determine the cell origin of sCD86. Methods: Serum sCD86 concentrations were measured in 52 asthmatic subjects and 25 non-atopic normal volunteers using an enzyme linked immunosorbent assay, and the relationship of serum sCD86 concentrations to asthma severity and to total and differential white cell counts was analysed. Each type of white blood cell was purified and cultured in vitro to determine the cell origin of serum sCD86. Results: Serum samples from patients with an acute asthma exacerbation had much higher levels of sCD86 (585.4 (20.5)IU/ml) than those from stable asthmatics (479.6 (15.7)IU/ml, p,0.001) and healthy individuals (435.1 (13.8)IU/ml, p,0.001), and there was no difference between the latter two groups (p=0.079). In asthmatic subjects the serum sCD86 level was inversely correlated with airway responsiveness, forced expiratory volume in 1 second, and with arterial carbon dioxide tension. In addition, the serum sCD86 level was positively correlated with numbers of lymphocytes, eosinophils, monocytes, but not neutrophils. The in vitro experiments indicated that sCD86 was produced by monocytes. Conclusions: The serum sCD86 protein level was significantly increased in asthmatic subjects during an exacerbation and correlated with the severity of asthma. sCD86 is most probably derived from monocytes in the peripheral blood.