International Immunology, Vol. 7, No. 3, pp. 449-457,March 1995
© 1995 Japanese Society for Immunology
IL-5 production by CD4+ T cells of asthmatic patients is suppressed by glucocorticoids and the immunosuppressants FK506 and cyclosporin A
Department of Medicine and Physical Therapy, University of Tokyo 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan
1 Suntory Institute for Biomedical Research Mishima, Osaka 618, Japan
Correspondence to: Correspondence to: H. Okudaira
IL-5 was produced in vitro by peripheral blood mononuclear cells (PBMC) of mite-sensitive atopic patients upon challenge with specific allergen, while PBMC of healthy controls produced essentially no IL-5. Stimuli delivered by the combination of phorbol ester and Ca2+ ionophore induced marked IL-5 production by PBMC obtained from atopic and non-atoplc asthmatics, suggesting that both protein kinase C and Ca2+ Influx are required for IL-5 production. CD2- or CD4-bearlng cell depletion almost completely removed IL-5-produclng cells while CD8-bearing cell depletion rather enriched them. These findings indicate that CD4+ T cells are the principal source of IL-5 in PBMC. The capacity of PBMC of atopic asthmatics, non-atopic asthmatics and healthy controls to produce IL-2, IL-4, IL-5 and IFN-
was compared, to find that cytokine-producing capacities other than that of IL-5 (IL-2, IL-4 and IFN-) were not significantly different among the three groups. Dexamethasone, FK506 and cyclosporin A suppressed IL-5 production in vitro in a dose-dependent manner. Clear dose-dependent suppression of IL-5 gene expression by FK506 was also observed. Treatment of asthmatic patients with inhaled glucocorticoid (beclomethasone dipropionate) ameliorated clinical symptoms, improved lung function and markedly suppressed IL-5 production by PBMC, suggesting the essential role of IL-5 in the pathogenesis of bronchial asthma and the clinical importance of its regulation.
Keywords: AP-1, bronchial asthma, cyclosporin, FK506, glucocorticoid, NF-AT, T cell
Received 27 December 1994, accepted 24 November 1994.
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