The Open Arthritis Journal
2010, 3 : 18-23Published online 2010 January 12. DOI: 10.2174/1876539401003010018
Publisher ID: TOARTHJ-3-18
RESEARCH ARTICLE
Macrophage Subsets in Immune-Mediated Inflammatory Disease: Lessons from Rheumatoid Arthritis, Spondyloarthritis, Osteoarthitis, Behçet’s
Disease and Gout
* Address correspondence to this author at the Academic Medical Center/University of Amsterdam, Division of Clinical Immunology and Rheumatology, K0-154, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands; Tel: +31 20 5667688; Fax: +31 20 6919658; E-mail: c.lebre@amc.uva.nl
ABSTRACT
Macrophages are a major cell population in most of the tissues, and their numbers increase massively in inflammation, in wound healing and in tumors. In particular, macrophages contribute to autoimmune events in rheumatic diseases, such as rheumatoid arthritis (RA) or spondyloarthritis (SpA), mainly acting as antigen-presenting cells and also as the major source of inflammatory mediators that are important in joint inflammation. In this respect, macrophages release a variety of pro-inflammatory cytokines and chemokines and events downstream of this cytokine cascade will contribute to cartilage and bone destruction. It is becoming clear that differential macrophage activation by distinct mechanisms is crucial for their function. This review will discuss several aspects of macrophage function in immune-mediated inflammatory disease with particular emphasis in RA, SpA, osteoarthitis, Behçet’s disease and gout.