Regulation of IgE production from human mononuclear cells by beta2-adrenoceptor agonists
Autor: | Jean Michel Mencia-Huerta, P. Braquet, O. Coqueret, B. Dugas |
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Rok vydání: | 1995 |
Předmět: |
medicine.medical_specialty
Cell Survival Lymphocyte medicine.medical_treatment Immunology Immunoglobulins Lymphocyte Activation Immunoglobulin E Peripheral blood mononuclear cell Monocytes Internal medicine Receptors Adrenergic beta Humans Immunology and Allergy Medicine Albuterol Fenoterol Lymphokines biology Receptors IgE business.industry CD23 Adrenergic beta-Agonists respiratory system medicine.anatomical_structure Endocrinology Cytokine Solubility Mechanism of action biology.protein Interleukin-4 medicine.symptom Antibody business medicine.drug |
Zdroj: | Clinical Experimental Allergy. 25:304-311 |
ISSN: | 1365-2222 0954-7894 |
DOI: | 10.1111/j.1365-2222.1995.tb01047.x |
Popis: | The present study examined the effect of beta 2-adrenoceptor agonists on the interleukin-4 (IL-4)-driven IgE production and on the possible mechanisms of action of these compounds. We present evidence that salbutamol and fenoterol potentiated the IL-4-induced IgE production by human peripheral blood mononuclear cells (PBMC). No significant effect of incubation in the presence of beta 2-adrenoceptor agonists on IgG, IgA and IgM production was observed. Salbutamol and fenoterol inhibited interferon-(IFN)-gamma production by PHA-activated human PBMC suggesting that the blockade of the production of this cytokine could possibly explain the enhancement of IgE production. Salbutamol and fenoterol potentiated the IL-4-induced production of sCD23 whereas no effect on CD23 expression was observed. The potentiating effect of salbutamol on IgE production was blocked by two antagonists of beta 2-adrenoceptor, namely butoxamine and D,L-propranolol, suggesting a beta-adrenoceptor-mediated event. These results demonstrate that beta 2-adrenoceptor stimulation results in an increase in IgE production by human B lymphocytes. |
Databáze: | OpenAIRE |
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