Receptor activator of NF-kappaB ligand enhances the activity of macrophages as antigen presenting cells.
- Author:
Hyewon PARK
1
;
Ok Jin PARK
;
Jieun SHIN
;
Youngnim CHOI
Author Information
1. Department of Oromaxillofacial Infection and Immunity and Dental Research Institute, School of Dentistry, Seoul National University, Seoul 110-749, Korea. youngnim@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
antigen presentation;
CD86 antigen;
cell survival;
cytokines;
macrophages;
MHC class II;
TRANCE protein
- MeSH:
Animals;
Antigen-Presenting Cells/cytology/*drug effects/immunology/*metabolism;
Antigens, CD86/metabolism;
Carrier Proteins/*pharmacology;
Cell Death/drug effects;
Cell Survival/drug effects;
Cells, Cultured;
Cytokines/metabolism;
Flow Cytometry;
Histocompatibility Antigens Class II/metabolism;
Inflammation Mediators;
Interferon Type II/pharmacology;
Lipopolysaccharides/pharmacology;
Macrophages/cytology/*drug effects/immunology/*metabolism;
Membrane Glycoproteins/*pharmacology;
Mice;
Mice, Inbred C57BL;
Mice, Inbred ICR;
Nitric Oxide Synthase Type II/metabolism;
Phagocytosis/drug effects;
Research Support, Non-U.S. Gov't;
T-Lymphocytes/immunology/metabolism;
Up-Regulation/drug effects/genetics
- From:Experimental & Molecular Medicine
2005;37(6):524-532
- CountryRepublic of Korea
- Language:English
-
Abstract:
Receptor activator of NFkappaB ligand (RANKL) is known as a key regulator of osteoclastogenesis. However, the fact that fibroblasts and periodontal ligament cells express RANKL in response to bacterial substances, suggests that RANKL may have evolved as a part of the immunity to infection. As RANKL increases the survival and activity of dendritic cells, it may have similar effects on macrophages. To address this issue, we studied the effect of RANKL on various functions of macrophages using mouse bone marrow derived macrophages. RANKL enhanced the survival of macrophages and up-regulated the expression of CD86. RANKL-treated macrophages showed increased allogeneic T cell activation and phagocytic activity compared to control cells. In addition, RANKL increased the expression of TNFalpha, MCP-1, and IL-6 but not of IL-10, IL-12, IFN-gamma, and iNOS. Collectively, RANKL augmented the activity of macrophages especially as antigen presenting cells, suggesting its new role in immune regulation.
