Kinne Raimund W, Stuhlmüller Bruno, Burmester Gerd-R
Experimental Rheumatology Unit, Department of Orthopedics, University Clinic, Jena, Klosterlausnitzer Str, 81, D-07607 Eisenberg, Germany.
Arthritis Res Ther. 2007;9(6):224. doi: 10.1186/ar2333.
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.
类风湿关节炎中巨噬细胞衍生介质的多样性和丰富性及其旁分泌/自分泌作用，表明巨噬细胞是疾病的局部和全身放大器。尽管揭示类风湿关节炎的病因仍是终止致病过程的最终手段，但了解活化巨噬细胞如何影响疾病的努力已促成了优化策略，即通过针对巨噬细胞活化特定特征量身定制的药物来选择性地靶向巨噬细胞。这种方法有两个优点：（a）针对介导/放大大部分不可逆组织破坏的细胞群体；（b）放过对关节损伤无（或仅有轻微）影响的其他细胞。
