Print Email Facebook Twitter Differential regulation of interleukin-10 (IL-10) and IL-12 by glucocorticoids in vitro Title Differential regulation of interleukin-10 (IL-10) and IL-12 by glucocorticoids in vitro Author Visser, J. van Boxel-Dezaire, A. Methorst, D. Brunt, T. de Kloet, E.R. Nagelkerken, L. TNO Preventie en Gezondheid Publication year 1998 Abstract Antigen-presenting cells are thought to modulate the development of Th1 and Th2 cells by the secretion of interleukin-10 (IL-10) and IL-12. Because glucocorticoids (GC) favor the development of Th2 responses, we determined whether dexamethasone (DEX) and hydrocortisone (HC) have differential effects on lipopolysaccharide-induced IL-10 and IL-12 production in whole-blood cultures. Significant inhibition of IL-12(p40) and IL-12(p70) was found with 10-8 mol/L and 10-9 mol/L DEX respectively, whereas IL-10 was relatively insensitive or even stimulated. Accordingly, the expression of IL-12(p40) and IL-12(p35) mRNA was more sensitive to DEX than IL-10 mRNA. The glucocorticoid receptor (GR) antagonist RU486 enhanced IL-12 production and largely abrogated the inhibition of IL-12 by GC, indicating that this suppression was mainly GR-mediated. High concentrations of RU486 were inhibitory for IL-10, suggesting that GC may exert a positive effect on IL-10. In the presence of neutralizing anti-IL-10 antibodies, DEX was still capable of IL-12 suppression whereas RU486 still enhanced IL-12 production, indicating that GC do not modulate IL-12 via IL-10 exclusively. Taken together these results indicate that GC may favor Th2 development by differential regulation of IL- 10 and IL-12. Subject HealthAntigen-Presenting CellsCells, CulturedDexamethasoneFemaleGlucocorticoidsHormone AntagonistsHumansHydrocortisoneInterleukin-10Interleukin-12LipopolysaccharidesMaleMifepristoneReceptors, GlucocorticoidRNA, MessengerTh1 CellsTh2 CellsTumor Necrosis Factor-alphaUp-Regulation To reference this document use: http://resolver.tudelft.nl/uuid:b3e12346-ca31-4686-84ed-0cd0286ab0b3 TNO identifier 234483 ISSN 0006-4971 Source Blood, 91 (11), 4255-4264 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.