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Article: Basophil histamine release and leukotriene production in response to anti-IgE and anti-IgE receptor antibodies: Comparison of normal subjects and patients with urticaria, atopic dermatitis or bronchial asthma

TitleBasophil histamine release and leukotriene production in response to anti-IgE and anti-IgE receptor antibodies: Comparison of normal subjects and patients with urticaria, atopic dermatitis or bronchial asthma
Authors
Issue Date1996
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/IAA
Citation
International Archives Of Allergy And Immunology, 1996, v. 110 n. 3, p. 261-271 How to Cite?
AbstractThe 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.
Persistent Identifierhttp://hdl.handle.net/10722/153960
ISSN
2015 Impact Factor: 2.677
2015 SCImago Journal Rankings: 1.164
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBischoff, SCen_US
dc.contributor.authorZwahlen, Ren_US
dc.contributor.authorStucki, Men_US
dc.contributor.authorMüllner, Gen_US
dc.contributor.authorDe Weck, ALen_US
dc.contributor.authorStadler, BMen_US
dc.contributor.authorDahinden, CAen_US
dc.date.accessioned2012-08-08T08:22:30Z-
dc.date.available2012-08-08T08:22:30Z-
dc.date.issued1996en_US
dc.identifier.citationInternational Archives Of Allergy And Immunology, 1996, v. 110 n. 3, p. 261-271en_US
dc.identifier.issn1018-2438en_US
dc.identifier.urihttp://hdl.handle.net/10722/153960-
dc.description.abstractThe 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.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/IAAen_US
dc.relation.ispartofInternational Archives of Allergy and Immunologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAntibodies, Anti-Idiotypic - Pharmacologyen_US
dc.subject.meshAntibodies, Monoclonal - Pharmacologyen_US
dc.subject.meshAsthma - Blood - Immunologyen_US
dc.subject.meshBasophils - Immunology - Metabolismen_US
dc.subject.meshDermatitis, Atopic - Blood - Immunologyen_US
dc.subject.meshDose-Response Relationship, Immunologicen_US
dc.subject.meshFemaleen_US
dc.subject.meshHistamine Releaseen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunoglobulin E - Blood - Immunologyen_US
dc.subject.meshInterleukin-3 - Pharmacologyen_US
dc.subject.meshLeukotrienes - Biosynthesisen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshReceptors, Ige - Immunologyen_US
dc.subject.meshUrticaria - Blood - Immunologyen_US
dc.titleBasophil histamine release and leukotriene production in response to anti-IgE and anti-IgE receptor antibodies: Comparison of normal subjects and patients with urticaria, atopic dermatitis or bronchial asthmaen_US
dc.typeArticleen_US
dc.identifier.emailZwahlen, R:zwahlen@hku.hken_US
dc.identifier.authorityZwahlen, R=rp00055en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8688673-
dc.identifier.scopuseid_2-s2.0-0029984053en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029984053&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume110en_US
dc.identifier.issue3en_US
dc.identifier.spage261en_US
dc.identifier.epage271en_US
dc.identifier.isiWOS:A1996UU30900009-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridBischoff, SC=7102810942en_US
dc.identifier.scopusauthoridZwahlen, R=7004217269en_US
dc.identifier.scopusauthoridStucki, M=8125684000en_US
dc.identifier.scopusauthoridMüllner, G=6602812659en_US
dc.identifier.scopusauthoridDe Weck, AL=7101983638en_US
dc.identifier.scopusauthoridStadler, BM=7102056649en_US
dc.identifier.scopusauthoridDahinden, CA=54790510300en_US

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