Cells of the synovium in rheumatoid arthritis. Macrophages
1 Experimental Rheumatology Unit, Department of Orthopedics, University Clinic, Jena, Klosterlausnitzer Str. 81, D-07607 Eisenberg, Germany
2 Department of Rheumatology and Clinical Immunology, Charité University Hospital, Humboldt University of Berlin, Tucholskystr. 2, D-10117 Berlin, Germany
Arthritis Research & Therapy 2007, 9:224 doi:10.1186/ar2333Published: 21 December 2007
The multitude and abundance of macrophage-derived mediators in rheumatoid arthritis and their paracrine/autocrine effects identify macrophages as local and systemic amplifiers of disease. Although uncovering the etiology of rheumatoid arthritis remains the ultimate means to silence the pathogenetic process, efforts in understanding how activated macrophages influence disease have led to optimization strategies to selectively target macrophages by agents tailored to specific features of macrophage activation. This approach has two advantages: (a) striking the cell population that mediates/amplifies most of the irreversible tissue destruction and (b) sparing other cells that have no (or only marginal) effects on joint damage.