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Modulation of macrophage differentiation and activation by decoy receptor 3
Author(s) -
Chang YungChi,
Hsu TsuiLing,
Lin HsiHsien,
Chio ChungChing,
Chiu Allen W.,
Chen NienJung,
Lin ChiHung,
Hsieh ShieLiang
Publication year - 2004
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0903448
Subject(s) - mannose receptor , biology , cd14 , cd16 , macrophage , microbiology and biotechnology , tumor necrosis factor alpha , immune system , cd11c , immunology , receptor , monocyte , cancer research , in vitro , phenotype , cd8 , cd3 , biochemistry , gene
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.