Effects of Dexamethasone on expressions of IFN-gamma and IL-4 by PBMCs in response to IL-12.
- Author:
Su Hak HEO
1
;
Seong Beom LEE
;
Gue Tae CHAE
Author Information
1. Institute of Hansen's disease, Department of Pathology, College of Medicine, The Catholic University of Korea, Korea.
- Publication Type:Original Article
- Keywords:
dexamethasone;
IL-12;
IFN-gamma;
IL-4
- MeSH:
Dexamethasone*;
Humans;
Interferons;
Interleukin-12*;
Interleukin-4*;
Receptors, Interleukin-12
- From:Korean Leprosy Bulletin
2002;35(2):3-12
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Dexamethasone is a widely used anti-inflammatory agent for a broad spectrum of diseases. The effectiveness of this agent is thought to be due to the capacity to modulate cytokine production in inflammatory cells. We examined the effects of dexamethasone on expressions of interferon gamma (IFN-gamma) and interleukin 4 (IL-4) by human peripheral blood mononuclear cells (PBMCs) in response to interleukin 12 (IL-12). Dexamethasone (10-5 M) inhibited IFN-gamma secretion, through direct suppression of IFN-gamma, IL-12 receptor (IL-12R) -beta1, and -beta2 expressions. Conversely dexamethasone increased IL-4 secretion as well as IL-4 expressions by PBMCs in response to IL-12. In addition, dexamethasone increased expression of suppressor of cytokine signalling (SOCS)-1, which inhibits JAK-STAT pathway of IL-12R signalling. The result of our study suggested that dexamethasone directly inhibited IFN-gamma expression, through suppression of IL-12 signalling and indirectly increases IL-4 expression, through suppression of IFN-gamma expression.
