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Blood, 15 July 2006, Vol. 108, No. 2, pp. 575-583.
Prepublished online as a Blood First Edition Paper on March 23, 2006; DOI 10.1182/blood-2005-04-1485.
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Submitted April 12, 2005
Accepted March 8, 2006
Identification of a common gene signature for type II cytokine-associated myeloid cells elicited in vivo during different pathologies
Gholamreza Hassanzadeh Ghassabeh, Patrick De Baetselier, Lea Brys, Wim Noel, Jo A Van Ginderachter, Sofie Meerschaut, Alain Beschin, Frank Brombacher, and Geert Raes*
Laboratory of Cellular and Molecular Immunology, Department of Molecular and Cellular Interactions, Vlaams Interuniversitair Instituut voor Biotechnologie, Vrije Universiteit Brussel, Brussels, Belgium
Health Sciences Faculty, University of Cape Town, Cape Town, South Africa
* Corresponding author; email: geerraes{at}vub.ac.be.
As compared with type I cytokine-associated myeloid cells (M1), the molecular repertoire and mechanisms underlying functional properties of type II cytokine-associated myeloid cells (M2) are poorly characterized. Moreover, most studies have been limited to in vitro-elicited M2. Here, comparative gene expression profiling of M1 and M2, elicited in murine models of parasitic infections and cancer, yielded a common signature for in vivo-induced M2 populations, which is independent of disease model, mouse strain and organ source of cells. Some of these genes, such as cadherin-1, selenoprotein P, platelet-activating factor acetylhydrolase and prosaposin, were not documented before to be associated with M2. Overall, the common signature genes provide a molecular basis for a number of documented or suggested properties of M2, including immunomodulation, down-regulation of inflammation, protection against oxidative damage, a high capacity for phagocytosis and tissue repair. Interestingly, several common M2 signature genes encode membrane-associated markers, which could be useful for identification and isolation of M2. Some of these genes were induced neither by IL-4/IL-13 nor by IL-10 under various in vitro settings, and thus would have been missed in approaches based on in vitro activated cells, validating our choice of in vivo models for expression profiling of myeloid cells.

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