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Originally published online as doi:10.1189/jlb.0903448 on December 4, 2003

Published online before print December 4, 2003
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(Journal of Leukocyte Biology. 2004;75:486-494.)
© 2004 by Society for Leukocyte Biology

Modulation of macrophage differentiation and activation by decoy receptor 3

Yung-Chi Chang*, Tsui-Ling Hsu*, Hsi-Hsien Lin{dagger}, Chung-Ching Chio{ddagger}, Allen W. Chiu{ddagger}, Nien-Jung Chen*, Chi-Hung Lin* and Shie-Liang Hsieh*,1

* Institute and Department of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan;
{dagger} Dunn School of Pathology, University of Oxford, United Kingdom; and
{ddagger} Department of Surgery, Chi-Mei Medical Center, Tainan, Taiwan

1Correspondence: Institute of Microbiology and Immunology, National Yang-Ming University, Shih-Pai, Taipei 112, Taiwan. E-mail: slhsieh{at}ym.edu.tw

Decoy receptor 3 (DcR3) is a soluble receptor of the tumor necrosis factor receptor superfamily and is readily detected in certain cancer patients. Recently, we demonstrated that DcR3.Fc-treated dendritic cells skew T cell responses to a T helper cell type 2 phenotype. In this study, we further asked its ability to modulate CD14+ monocyte differentiation into macrophages induced by macrophage-colony stimulating factor in vitro. We found that DcR3.Fc was able to modulate the expression of several macrophage markers, including CD14, CD16, CD64, and human leukocyte antigen-DR. In contrast, the expression of CD11c, CD36, CD68, and CD206 (mannose receptor) was not affected in the in vitro culture system. Moreover, phagocytic activity toward immune complexes and apoptotic bodies as well as the production of free radicals and proinflammatory cytokines in response to lipopolysaccharide were impaired in DcR3.Fc-treated monocyte-derived macrophages. This suggests that DcR3.Fc might have potent, suppressive effects to down-regulate the host-immune system.

Key Words: tumor necrosis factor • phagocytosis • apoptosis • inflammation




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