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Volume 78, Issue 2, Pages 140-148 (July 2008)


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IL-13 induces the expression of the alternative activation marker Ym1 in a subset of testicular macrophages

Katarzyna Maresza1, Eugene D. Ponomareva1, Natasha Bartenevab, Yanping Tana, Monica K. Mannac, Bonnie N. DittelacCorresponding Author Informationemail address

Received 5 April 2007; received in revised form 20 October 2007; accepted 15 January 2008. published online 10 March 2008.

Abstract 

Macrophages are thought to play an important role in the maintenance of immune privilege in the testis, which functions to prevent immune responses to developing sperm. Two populations of macrophages are known to exist in the testis, one of which exhibits immunosuppressive activity. Macrophages that are alternatively activated with either IL-4 or IL-13 have been shown to be anti-inflammatory and promote wound healing. Expression of the Ym1 protein is an established marker of alternatively activated macrophages. Testicular macrophages were examined for expression of Ym1 protein, and it was found to be highly expressed in a subpopulation of CD11b+ cells. Furthermore, we have shown that Ym1 protein expression in the testis is dependent upon IL-13R signaling, and that IL-13 is produced in the testis. These data suggest that IL-13 plays a role in testicular immune privilege by the maintenance of an alternatively activated macrophage population.

a BloodCenter of Wisconsin, Blood Research Institute, 8727 Watertown Plank Road, Milwaukee, WI 53226, USA

b Flow and Imaging Cytometry Facility, Immune Disease Institute, Harvard Medical School, Boston, MA 02115, USA

c Department of Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, WI 53226, USA

Corresponding Author InformationCorresponding author at: BloodCenter of Wisconsin, Blood Research Institute, 8727 Watertown Plank Road, P.O. Box 2178, Milwaukee, WI 53226, USA. Tel.: +1 414 937 3865; fax: +1 414 937 6284.

1 These authors contributed equally to this work.

PII: S0165-0378(08)00004-1

doi:10.1016/j.jri.2008.01.001


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