C-reactive protein functions as a negative regulator of macrophage activation induced by apoptotic DNA.
10.1007/s13238-011-1084-4
- Author:
Weijuan ZHANG
1
;
Yanxing CAI
;
Wei XU
;
Sidong XIONG
Author Information
1. Institute for Immunobiology and Department of Immunology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
- Publication Type:Journal Article
- MeSH:
Animals;
C-Reactive Protein;
metabolism;
pharmacology;
Cell Line, Tumor;
DNA;
metabolism;
pharmacology;
Enzyme-Linked Immunosorbent Assay;
Female;
Lupus Erythematosus, Systemic;
metabolism;
Lupus Nephritis;
metabolism;
Macrophage Activation;
drug effects;
physiology;
Mice;
Mice, Inbred BALB C;
Protein Binding;
Real-Time Polymerase Chain Reaction
- From:
Protein & Cell
2011;2(8):672-679
- CountryChina
- Language:English
-
Abstract:
C-reactive protein (CRP), an acute-phase protein with an ability to bind to nuclear antigen, has been reported to regulate cytokine secretion and modulate immune responses. We previously reported that activated syngeneic lymphocyte-derived apoptotic DNA (apopDNA) could induce macrophage activation and contribute to the initiation and progression of lupus nephritis. It is reasonable to hypothesize that CRP might regulate apopDNA-induced macrophage activation. Herein, CRP was shown to promote macrophage-mediated apopDNA uptake by binding to apopDNA (CRP/apopDNA complex). Notably, CRP/apopDNA treatment inhibited the production of inflammatory cytokines and chemokines by macrophages which could be induced by apopDNA alone. Further coculture and transwell studies revealed that CRP/apopDNA-induced macrophages prohibited apopDNA-induced macrophage activation in an IL-10 dependent manner. These results provide insight into the potential mechanism of CRP regulatory activity in macrophage activation induced by apopDNA in the context of lupus nephritis and other autoimmune diseases.
