Müller-Ladner U, Kriegsmann J, Franklin B N, Matsumoto S, Geiler T, Gay R E, Gay S
Division of Clinical Immunology, University of Alabama at Birmingham, USA.
Am J Pathol. 1996 Nov;149(5):1607-15.
Rheumatoid arthritis (RA) has been thought to be largely a T-cell-mediated disease. To evaluate the role of T-cell-independent pathways in RA, we examined the interaction between isolated RA synovial fibroblasts and normal human cartilage engrafted into SCID mice in the absence of T cells and other human cells. The expression of cartilage-de grading enzymes and adhesion molecules was examined by immunohistochemistry and in situ hybridization techniques. The RA synovial fibroblasts invaded the cartilage and kept their transformed appearing cellular shape. They expressed VCAM-1 and produced the cathepsins L and B at the site of invasion. We conclude that RA synovial fibroblasts maintain their invasive and destructive behavior over longer periods of time in the absence of human T cells, indicating that T-cell-independent pathways play a significant role in rheumatoid joint destruction.
类风湿性关节炎（RA）一直被认为主要是一种由T细胞介导的疾病。为了评估T细胞非依赖途径在类风湿性关节炎中的作用，我们在无T细胞及其他人类细胞的情况下，研究了分离出的类风湿性关节炎滑膜成纤维细胞与移植到SCID小鼠体内的正常人软骨之间的相互作用。通过免疫组织化学和原位杂交技术检测软骨降解酶和黏附分子的表达。类风湿性关节炎滑膜成纤维细胞侵入软骨并保持其转化后的细胞形态。它们在侵入部位表达血管细胞黏附分子-1（VCAM-1）并产生组织蛋白酶L和B。我们得出结论，在无人类T细胞的情况下，类风湿性关节炎滑膜成纤维细胞在较长时间内维持其侵袭性和破坏性行为，这表明T细胞非依赖途径在类风湿性关节破坏中起重要作用。
