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Originally published online as doi:10.1189/jlb.0207092 on July 11, 2007

Published online before print July 11, 2007
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(Journal of Leukocyte Biology. 2007;82:926-933.)
© 2007 by Society for Leukocyte Biology

Chorionic gonadotropin can enhance innate immunity by stimulating macrophage function

Hui Wan1, Marjan A. Versnel, Wai yee Cheung, Pieter J. M. Leenen, Nisar A. Khan, Robbert Benner and Rebecca C. M. Kiekens

Department of Immunology, Erasmus MC, Rotterdam, The Netherlands

1 Correspondence: Department of Immunology, Erasmus MC, Dr. Molewaterplein 50, NL-3015 GE Rotterdam, The Netherlands. E-mail: h.wan{at}erasmusmc.nl

Human chorionic gonadotropin (hCG) is a placental glycoprotein, mainly secreted by trophoblasts during pregnancy. Its function in endocrine regulation has been well documented, but its immunological role is still largely unclear. For a successful pregnancy, an effective innate immunity is needed to protect the mother and fetus against infection, while maintaining tolerance against the paternal antigens of the fetus. The aim of this study was to investigate the effect of hCG on the function of macrophages (M{varphi}), which are major players in the innate response. hCG treatment of IFN-{gamma}-primed M{varphi} resulted in increased production of NO, reactive oxygen species, IL-6 and IL-12p40, and enhanced phagocytosis of apoptotic cells. hCG treatment did not affect the induction of allogeneic T cell proliferation by IFN-{gamma}-primed M{varphi}. The observed effects were receptor-mediated and involved the protein kinase A signaling pathway, as indicated by blocking studies using specific inhibitors. In vivo thioglycollate-elicited M{varphi} also exhibited increased phagocytic ability upon IFN-{gamma} activation and hCG treatment. In conclusion, hCG enhances M{varphi} functions involved in innate immunity, while the capacity to stimulate allogeneic T cells remains unchanged.

Key Words: hCG • M{varphi} • ROS • phagocytosis




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H. Wan, C. G. van Helden-Meeuwsen, C. Garlanda, L. M. E. Leijten, V. Maina, N. A. Khan, H. A. Drexhage, A. Mantovani, R. Benner, and M. A. Versnel
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