OBJECTIVE: We aimed to assess the percentage of peripheral blood B-lymphocytes expressing OX40 ligand (OX40L) in adult atopic and non-atopic asthmatic patients, and in healthy controls. METHODS: This case-control study included 15 atopic asthmatic patients, 15 non-atopic asthmatic patients, and 15 healthy controls. Atopic status was determined by skin prick test reaction to the most common locally-encountered allergens. For all subjects, pulmonary function tests and measurement of total serum immunoglobulin E (IgE) levels by ELISA were performed. In addition, the percentage of B-lymphocytes expressing OX40L was assessed by flow cytometry in all three groups. RESULTS: OX40L expression was significantly higher in atopic asthmatics than in non-atopic asthmatics and controls, but did not differ significantly between non-atopic asthmatics or controls. Among atopic asthmatics, OX40L expression correlated positively with total serum IgE levels, but not with age, disease duration, or values of forced expiratory volume in the first second. CONCLUSION: The over-expression of OX40L in atopic asthmatic patients appears to be linked to markers of the atopic status as total serum IgE, and signifies the vital role of OX40L in the atopic mechanism. Further large-scale studies are needed to investigate the role of OX40L in other atopic diseases and its relation to disease activity and severity.
OBJECTIVE: We aimed to assess the percentage of peripheral blood B-lymphocytes expressing OX40 ligand (OX40L) in adult atopic and non-atopic asthmatic patients, and in healthy controls. METHODS: This case-control study included 15 atopic asthmatic patients, 15 non-atopic asthmatic patients, and 15 healthy controls. Atopic status was determined by skin prick test reaction to the most common locally-encountered allergens. For all subjects, pulmonary function tests and measurement of total serum immunoglobulin E (IgE) levels by ELISA were performed. In addition, the percentage of B-lymphocytes expressing OX40L was assessed by flow cytometry in all three groups. RESULTS:OX40L expression was significantly higher in atopic asthmatics than in non-atopic asthmatics and controls, but did not differ significantly between non-atopic asthmatics or controls. Among atopic asthmatics, OX40L expression correlated positively with total serum IgE levels, but not with age, disease duration, or values of forced expiratory volume in the first second. CONCLUSION: The over-expression of OX40L in atopic asthmatic patients appears to be linked to markers of the atopic status as total serum IgE, and signifies the vital role of OX40L in the atopic mechanism. Further large-scale studies are needed to investigate the role of OX40L in other atopic diseases and its relation to disease activity and severity.