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Blood, 1 February 2007, Vol. 109, No. 3, pp. 1265-1274.
Prepublished online as a Blood First Edition Paper on October 3, 2006; DOI 10.1182/blood-2006-02-001115.
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PHAGOCYTES
Glucocorticoids induce differentiation of a specifically activated, anti-inflammatory subtype of human monocytes
Jan Ehrchen1,2,3,
Lars Steinmüller1,
Katarzyna Barczyk1,
Klaus Tenbrock1,2,4,
Wolfgang Nacken1,2,
Martin Eisenacher2,
Ursula Nordhues1,
Clemens Sorg1,2,
Cord Sunderkötter3, and
Johannes Roth1,2,4
1 Institute of Experimental Dermatology, University of Muenster, Germany;
2 Interdisciplinary Centre for Clinical Research, University of Muenster, Germany;
3 Department of Dermatology, University of Muenster, Germany;
4 Department of Pediatrics, University of Muenster, Germany
Monocytes and macrophages may either promote or down-regulate inflammatory reactions depending on their state of activation. The effects of glucocorticoids (GCs), the most widely used immunosuppressive drugs, on monocytes are currently not well defined. By analyzing the GC-induced expression pattern in human monocytes by microarray technology, we identified for the first time GC-dependent regulation of 133 genes, including anti-inflammatory molecules such as adenosine A3 receptor, CD1d, and IL-1 receptor II. The results were independently confirmed by real-time polymerase chain reaction (PCR) and flow cytometry. Functional clustering of GC-regulated genes indicated induction of monocytic properties such as phagocytosis and motility as well as repression of adhesion, apoptosis, and oxidative burst. These predictions were confirmed by independent functional assays. GCs up-regulate fMLP receptors and specifically promote chemotaxis to this chemoattractant. Furthermore, GCs promote survival of an anti-inflammatory monocytic phenotype in inflammatory reactions, probably by inhibition of apoptosis because of oxidative stress. GCs limit tissue damage because of induction of antioxidative properties and high capacity for phagocytosis of proinflammatory agents. Thus, GC treatment did not cause a global suppression of monocytic effector functions but results in differentiation of a specific anti-inflammatory phenotype which seems to be actively involved in resolution of inflammatory reactions.
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