Telfer Joan F, Brock Jeremy H
Department of Immunology, Western Infirmary, University of Glasgow, United Kingdom.
Med Sci Monit. 2004 Apr;10(4):BR91-5.
It has been hypothesized that iron is stored in the synovium of patients with rheumatoid arthritis which perpetuates inflamation by aiding the production of oxygen free radicals. Proinflammatory cytokines are produced by macrophages and lymphocytes present within synovium and by mononuclear cells of in synovial fluid from patients with rheumatoid arthritis. There are two known systems for iron uptake. The first involves binding of iron to transferrin and uptake via transferrin receptors. The second involves uptake by low molecular weight organic anions such as ascorbate and citrate (non-transferrin bound uptake).
MATERIALS/METHODS: Proinflammatory cytokines (IL-1, IL-6, TNFalpha and interferon gamma) were added to fibroblasts isolated from patients with rheumatoid arthritis and human monocytes in culture and their effect on 59Fe-transferrin and citrate uptake was determined.
Proinflammatory cytokines increase transferrin and non-transferrin bound iron uptake into human monocytes and increase transferrin-bound iron uptake by synovial fibroblasts, but have no effect on non-transferrin bound uptake into fibroblasts.
Proinflammatory cytokines produced in human rheumatoid arthritis synovium and synovial fluid may contribute to the accumulation of iron that occurs in rheumatoid arthritis synovium which may lead to damage to synovial fibroblasts, macrophages and lymphocytes.
据推测，类风湿关节炎患者的滑膜中储存有铁，铁通过促进氧自由基的产生使炎症持续存在。类风湿关节炎患者滑膜内的巨噬细胞和淋巴细胞以及滑膜液中的单核细胞可产生促炎细胞因子。已知有两种铁摄取系统。第一种是铁与转铁蛋白结合并通过转铁蛋白受体摄取。第二种是通过低分子量有机阴离子如抗坏血酸盐和柠檬酸盐摄取（非转铁蛋白结合摄取）。
材料/方法：将促炎细胞因子（白细胞介素-1、白细胞介素-6、肿瘤坏死因子α和干扰素γ）添加到从类风湿关节炎患者分离的成纤维细胞和培养的人单核细胞中，测定其对59Fe-转铁蛋白和柠檬酸盐摄取的影响。
促炎细胞因子增加人单核细胞中转铁蛋白和非转铁蛋白结合的铁摄取，并增加滑膜成纤维细胞中转铁蛋白结合的铁摄取，但对成纤维细胞中非转铁蛋白结合的摄取没有影响。
类风湿关节炎滑膜和滑膜液中产生的促炎细胞因子可能导致类风湿关节炎滑膜中铁的积累，这可能会导致滑膜成纤维细胞、巨噬细胞和淋巴细胞受损。
