Basophil Histamine Release and Leukotriene Production in Response to Anti-IgE and Anti-IgE Receptor Antibodies
| Autor: | Stephan C. Bischoff, M Stucki, A.L. de Weck, Roger A. Zwahlen, Clemens A. Dahinden, Beda M. Stadler, G. Müllner |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
medicine.medical_specialty
Allergy Immunology chemical and pharmacologic phenomena Basophil Immunoglobulin E Atopy chemistry.chemical_compound Internal medicine parasitic diseases medicine Immunology and Allergy Leukotriene biology business.industry hemic and immune systems General Medicine Atopic dermatitis medicine.disease Endocrinology medicine.anatomical_structure chemistry biology.protein Antibody business Histamine |
| Zdroj: | International Archives of Allergy and Immunology. 110:261-271 |
| ISSN: | 1423-0097 1018-2438 |
| DOI: | 10.1159/000237297 |
| Popis: | The IgE receptor-dependent in vitro mediator release in basophils is characterized by a large interindividual variability both in normal and atopic subjects. The mechanism and the clinical impact of this finding, however, is largely unclear. The aim of the present study was to examine the role of surface-bound IgE and of response-modifying cytokines such as interleukin 3 (IL-3) as possible factors determining basophil releasability in atopic patients and normal controls. Cells from 30 individuals (6 with urticaria, 7 with asthma, 7 with atopic dermatitis, and 30 healthy controls) were isolated and stimulated for mediator release by IL-3 and different triggering antibodies directed against IgE or IgE receptor. Our data suggest that serum IgE levels and basophil receptor occupancy with IgE are not involved in the mechanism of basophil releasability. Furthermore, IL-3-induced similar effects on mediator release in almost all individuals, rather excluding the possibility that releasability is regulated by cytokine priming of basophils. Interestingly, we found that patients with atopic disease have a reduced capacity of releasing mediators upon activation, the mechanism of which is unclear. In conclusion, our findings support the hypothesis that basophil releasability is dependent on cell-immanent mechanisms in basophils, which may be altered in selected atopic patients. |
| Databáze: | OpenAIRE |
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