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Comparison of IL-17 Production by Helper T Cells among Atopic and Nonatopic Asthmatics and Control SubjectsHashimoto T.a · Akiyama K.a · Kobayashi N.b · Mori A.a
aClinical Research Center for Allergy and Rheumatology, National Sagamihara Hospital, Sagamihara, Kanagawa, and bDepartment of Biotechnology, Tokyo Technical College, Kunitachi, Tokyo, Japan
Background: T cells, eosinophils, and neutrophils are strongly involved in the pathogenesis of bronchial asthma. Mechanisms that influence neutrophil accumulation and activation in asthma still remain relatively obscure. There is data indicating that IL-17 is produced by T cells and causes the release of neutrophil-mobilizing cytokines from airway epithelial cells, and that in this way it may regulate airway neutrophilia. Methods: Peripheral blood mononuclear cells (PBMC) obtained from atopic asthmatics (AA), nonatopic asthmatics (NA), and normal control subjects (NC) were stimulated by immobilized anti-CD3 antibody (Ab) plus soluble anti-CD28 Ab or Dermatophagoidesfarinae (Df) extract. Df-reactive T cell clones were established from PBMC of AA and cultured in the presence of various stimulants. The resulting supernatants were assayed for IL-2, IL-4, IL-5, IL-13, IL-17, and IFN-γ by specific ELISAs. Results: PBMC obtained from AA, NA, and NC all produced IL-17 upon immobilized anti-CD3 Ab plus soluble anti-CD28 Ab stimulation. IL-17 production in response to Df extract was significantly induced only in AA. The amount of IL-17 produced by T cell clones stimulated with immobilized anti-CD3 Ab plus soluble anti-CD28 Ab was negatively, but only weakly, correlated with that of IL-4, but not correlated with IL-2, IL-5, IL-13, and IFN-γ production. Conclusion: T cells producing IL-17 in response to Df antigen exist in the peripheral blood of the sensitized AA. IL-17 production might be regulated by unique mechanisms different from those governing Th1 versus Th2 differentiation.
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