The Soluble Form of the Cellular Prion Protein Enhances Phagocytic Activity and Cytokine Production by Human Monocytes Via Activation of ERK and NF-kappaB.
- Author:
Jae Won JEON
1
;
Bum Chan PARK
;
Joon Goo JUNG
;
Young Soon JANG
;
Eui Cheol SHIN
;
Young Woo PARK
Author Information
- Publication Type:Original Article
- Keywords: Soluble PrP(C); Phagocytosis; Adherence; Pro-inflammatory cytokine; Signaling
- MeSH: Cytokines; Humans; Immunoglobulin G; Interleukin-6; Macrophages; Monocytes; NF-kappa B; Phagocytosis; Tumor Necrosis Factor-alpha
- From:Immune Network 2013;13(4):148-156
- CountryRepublic of Korea
- Language:English
- Abstract: The PrP(C) is expressed in many types of immune cells including monocytes and macrophages, however, its function in immune regulation remains to be elucidated. In the present study, we examined a role for PrP(C) in regulation of monocyte function. Specifically, the effect of a soluble form of PrP(C) was studied in human monocytes. A recombinant fusion protein of soluble human PrP(C) fused with the Fc portion of human IgG1 (designated as soluble PrP(C)-Fc) bound to the cell surface of monocytes, induced differentiation to macrophage-like cells, and enhanced adherence and phagocytic activity. In addition, soluble PrP(C)-Fc stimulated monocytes to produce pro-inflammatory cytokines such as TNF-alpha, IL-1beta, and IL-6. Both ERK and NF-kappaB signaling pathways were activated in soluble PrP(C)-treated monocytes, and inhibitors of either pathway abrogated monocyte adherence and cytokine production. Taken together, we conclude that soluble PrP(C)-Fc enhanced adherence, phagocytosis, and cytokine production of monocytes via activation of the ERK and NF-kappaB signaling pathways.
