Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 21 S4.2

Institute of Immunology, University of Münster, Münster, Germany.


Active resolution of inflammation is a previously unrecognized process essential for tissue homeostasis. 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 and functional clustering we demonstrate that GC induce monocytic properties such as phagocytosis and motility as well as repression of adhesion, apoptosis, and oxidative burst. Furthermore, we demonstrate that GCs exhibit anti-apoptotic effects in monocytes resulting in differentiation to an anti-inflammatory phenotype. The molecular basis of this novel anti-apoptotic effect is a prolonged activation of the ERK/MAPK pathway resulting in inhibition of caspase activities and expression of anti-apoptotic genes via activation of c-Myc. We identified up-regulation and activation of A3 adenosine receptor (A3AR) as the initial trigger of this anti-apoptotic pathway. In summary we deciphered a novel molecular pathway promoting survival of anti-inflammatory monocytes, which results in differentiation of a specific anti-inflammatory phenotype actively involved in resolution of inflammatory reactions.

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