Corticosteroid modulation of human, antigen-specific Th1 and Th2 responses - 10/09/11
Abstract |
Corticosteroids are potent antiinflammatory agents that modulate human T-lymphocyte responses. Controversy remains as to their possible differential effects on Th1 and Th2 subsets. This study explores the kinetics and efficacy of these agents in human, antigen-driven peripheral blood mononuclear cells (PBMCs) and in nontransformed, antigen-specific Th1 and Th2 clones. Ragweed- and tetanus toxoid–driven proliferative responses of PBMCs from dually sensitized individuals were downregulated equally by dexamethasone (inhibitory concentration of 50% [IC50] = 3 × 10–9 and 2 × 10–9 mol/L, respectively). The addition of dexamethasone as late as 36 hours after ragweed stimulation still resulted in more than 75% inhibition of the proliferative response, whereas the efficacy of dexamethasone was less than 50% when added 24 hours after tetanus toxoid stimulation. Antigen-induced gene expression for proinflammatory cytokines (IL-4, IL-5, IL-13, and interferon-γ) from PBMCs was also downregulated by dexamethasone. Proliferation of antigen-specific Th1 and Th2 clones was inhibited by several corticosteroids (hydrocortisone < budesonide < dexamethasone; IC50 = 10–6 to 10–8 mol/L), but no significant differences between Th1 and Th2 clones were evident. IC50 values in the clones were 10-fold greater than in PBMCs. Gene expres-sion and protein secretion for IL-4, IL-13, and interferon-γ were downregulated in a concentration-dependent manner by each of the corticosteroids in Th1 and Th2 clones. These data suggest that Th1 and Th2 responses are equally affected by corticosteroids. (J Allergy CLin Immunol 1997;100:400-7.)
Le texte complet de cet article est disponible en PDF.Keywords : Human, Th1/Th2, IL-4, IL-13, interferon-γ, corticosteroids
Abbreviations : APCs, IC50, IFN, PBMCs, RT-PCR, RW, TT
Plan
From the Division of Clinical Immunology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore. |
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Supported by grants AI07290 and AI34002 of the National Institute of Allergy and Infectious Diseases, National Institutes of Health, and a Research Fellowship Award from the American Lung Association. |
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Reprint requests: David M. Essayan, MD, Johns Hopkins Asthma and Allergy Center, Rm 1A12, 5501 Hopkins Bayview Circle, Baltimore, MD 21224. |
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Vol 100 - N° 3
P. 400-407 - septembre 1997 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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