Receptor activator of NF-kappaB ligand enhances the activity of macrophages as antigen presenting cells

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...

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Bibliographic Details
Published in:Experimental & molecular medicine 2005-12, Vol.37 (6), p.524-532
Main Authors: Park, Hyewon Jin, Park, Ok Jin, Shin, Jieun
Format: Article
Language:English
Subjects:
Animals
Antigen-Presenting Cells - cytology
Antigen-Presenting Cells - drug effects
Antigen-Presenting Cells - immunology
Antigen-Presenting Cells - metabolism
B7-2 Antigen - 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-gamma - pharmacology
Lipopolysaccharides - pharmacology
Macrophages - cytology
Macrophages - drug effects
Macrophages - immunology
Macrophages - metabolism
Membrane Glycoproteins - pharmacology
Mice
Mice, Inbred C57BL
Mice, Inbred ICR
Nitric Oxide Synthase Type II - metabolism
Phagocytosis - drug effects
RANK Ligand
Receptor Activator of Nuclear Factor-kappa B
T-Lymphocytes - immunology
T-Lymphocytes - metabolism
Up-Regulation - drug effects
Up-Regulation - genetics
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Summary: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.
ISSN:1226-3613