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IL-5-producing T cells that induce airway eosinophilia and hyperresponsiveness are suppressed by dexamethasone and cyclosporin A in mice.
- Source :
-
International archives of allergy and immunology [Int Arch Allergy Immunol] 1998 Sep; Vol. 117 Suppl 1, pp. 24-7. - Publication Year :
- 1998
-
Abstract
- We have recently demonstrated that airway eosinophilic inflammation can be transferred to unprimed mice by infusion of IL-5-producing T cell clones. In this study, we investigated the effects of dexamethasone and cyclosporin A on the airway eosinophilic inflammation in mice transferred with T cell clones. An ovalbumin-reactive T cell clone, KW29, produced IL-5 as well as IL-2 and IL-4 upon stimulation with relevant antigen. Dexamethasone and cyclosporin A dose-dependently suppressed the production of these cytokines in vitro. The number of eosinophils recovered in the bronchoalveolar lavage fluid and the airway responsiveness to acetylcholine were increased in KW29-transferred mice after antigen provocation. Both responses were dose-dependently suppressed by the administration of dexamethasone or cyclosporin A in vivo. We concluded that airway eosinophilic inflammation can be controlled by agents capable of downregulating IL-5 production in T cells.
- Subjects :
- Adoptive Transfer
Animals
Bronchial Hyperreactivity immunology
Bronchial Hyperreactivity prevention & control
Clone Cells
Eosinophilia immunology
Eosinophilia prevention & control
Immunosuppressive Agents pharmacology
Mice
Mice, Inbred BALB C
Ovalbumin immunology
Respiratory Tract Diseases etiology
Respiratory Tract Diseases immunology
Respiratory Tract Diseases prevention & control
Bronchial Hyperreactivity etiology
CD4-Positive T-Lymphocytes drug effects
CD4-Positive T-Lymphocytes immunology
Cyclosporine pharmacology
Dexamethasone pharmacology
Eosinophilia etiology
Interleukin-5 biosynthesis
Subjects
Details
- Language :
- English
- ISSN :
- 1018-2438
- Volume :
- 117 Suppl 1
- Database :
- MEDLINE
- Journal :
- International archives of allergy and immunology
- Publication Type :
- Academic Journal
- Accession number :
- 9758892
- Full Text :
- https://doi.org/10.1159/000053566