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Published on: June 23, 2013
Modulation of macrophage differentiation and activation by decoy receptor 3
Yung-Chi Chang1, Tsui-Ling Hsu, Hsi-Hsien Lin
1Institute and Department of Microbiology and Immunology, National Yang-Ming University, Shih-Pai, Taipei 112, Taiwan.
Abstract:
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.
Insights
Decoy receptor 3 (DcR3) suppresses immune responses by impairing monocyte-derived macrophage function. This soluble receptor affects macrophage marker expression and reduces their ability to clear cellular debris and produce inflammatory cytokines.
Area of Science:
- Immunology
- Cell Biology
Background:
- Decoy receptor 3 (DcR3) is a soluble receptor in the tumor necrosis factor receptor superfamily.
- DcR3 is detected in cancer patients and can influence T cell responses.
Purpose of the Study:
- To investigate the effect of DcR3.Fc on the differentiation of CD14+ monocytes into macrophages.
- To determine how DcR3.Fc modulates macrophage characteristics and functions.
Main Methods:
- Monocyte differentiation into macrophages was induced using macrophage-colony stimulating factor in vitro.
- Flow cytometry was used to analyze the expression of various macrophage markers.
- Phagocytic activity and cytokine production were assessed in DcR3.Fc-treated macrophages.
Main Results:
- DcR3.Fc modulated the expression of macrophage markers including CD14, CD16, CD64, and human leukocyte antigen-DR.
- Expression of CD11c, CD36, CD68, and CD206 (mannose receptor) remained unaffected.
- Phagocytosis and the production of free radicals and proinflammatory cytokines were impaired in DcR3.Fc-treated macrophages.
Conclusions:
- DcR3.Fc influences monocyte differentiation into macrophages.
- DcR3.Fc exhibits suppressive effects on macrophage function, potentially down-regulating the host immune system.
