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dc.contributor.authorConesa, Angela-
dc.contributor.authorTassinari, Paolo-
dc.contributor.authorAldrey, Oscar-
dc.contributor.authorTaylor, Peter-
dc.contributor.authorBianco Colmenares, Nicolás E.-
dc.contributor.authorDe Sanctis, Juan B.-
dc.date.accessioned2017-03-14T19:35:05Z-
dc.date.available2017-03-14T19:35:05Z-
dc.date.issued2003-
dc.identifier.issn1539-6304 (Electronic)-
dc.identifier.issn1088-5412 (Linking)-
dc.identifier.issn1088-5412 (Print)-
dc.identifier.urihttp://hdl.handle.net/10872/15122-
dc.description.abstractIn this study we assessed, by flow cytometry, the effect of interleukin 2 (IL-2) on the oxidative burst of normodense eosinophils (Eos's) isolated from 15 patients with moderately severe extrinsic asthma and 17 controls. We found that IL-2 significantly induced peroxide (H2O2) production in normodense Eos's from patients with asthma on a time kinetics study. This rise was higher in patients with immunoglobulin E levels > 180 IU/mL versus normal immunoglobulin E values. The effect of IL-2 was partially blocked by using anti-Tac antibody. In contrast, IL-2 decreased H2O2 production in normodense Eos's from controls. Cell surface expression of CD25, CD122, CD132, and CD69 were also determined and no statistical differences were found between both groups. In conclusion, IL-2 is able to increase H2O2 production by normodense Eos's isolated from patients with asthma and it may contribute to bronchial epithelium damage and chronic inflammation.en_US
dc.language.isoenen_US
dc.publisherAllergy and asthma proceedingsen_US
dc.relation.ispartofseriesVol. 24;No. 1 pp 27-33-
dc.subjectinterleukin 2en_US
dc.subjectPeroxide Productionen_US
dc.subjectAsthmaen_US
dc.subjectIL-2en_US
dc.subjectimmunoglobulin Een_US
dc.subjectbronchial epitheliumen_US
dc.titleInterleukin-2 induces peroxide production by primed normodense eosinophils of patients with asthma.en_US
dc.typeArticleen_US
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