The role of rheumatoid factor on altered immune responses of intra-articular lymhocytes in rheumatoid arthritis.

本文检测了类风湿关节炎（RA）患者的关节液（SF）和血清（S）中IgM、IgM类风湿因子（IgM-RF）。白蛋白和白细胞介素-6（IL-6）活性。7例血清学阳性RA患者SFISIGN-RF与SF/S白蛋白的比值均高于SF/S白蛋白，但SF/S IgN比值低于SF/S白蛋白。7例RA患者SF IL-6活性均高于血清IL-6活性。在22例血清阳性RA患者的滑液中，SF IL-6活性与SF I gill-RF显著相关。IGG-RF和IGA-RF，但不与SF[gM]、[gG]或伊加。此外，SF IGM-RF以及SF IL-6活性与Westergren红细胞沉降率（ESR）或Lansbury关节指数显著相关。提示类风湿关节炎关节内可能由于免疫系统的异常激活而产生β-L-6和RF，并与疾病活动有关。4例血清阴性RA患者中有3例 关于我们 然而，患者显示高SF IL-6，但未检测到SF IGM-RF水平。为探讨类风湿关节炎（RA）患者外周血单个核细胞表面CD 14、Fc γ受体1（Fc γ RI）、FcrRH和HLA-DR的表达及其在RA发病中的作用，我们对9例RA患者外周血单个核细胞表面CD 14、Fc γ RI、FcrRH和HLA-DR的表达进行了研究。1类风湿性滑膜炎的病因。取9例活动期RA患者、8例完全缓解期RA患者和14例健康人外周血单个核细胞，用各种单克隆抗体染色，用荧光激活细胞分选仪分析。活动期RA患者外周血单个核细胞CD 14、Fc γ R Ⅰ和Fc γ R Ⅱ表达上调，HLA-DR表达无明显变化。此外，在RA完全缓解患者中，单核细胞上的Fc γ RI和Fc RII的表达仍上调，而这些患者中，单核细胞上的CD 14的表达正常化。这些结果表明，活动性RA患者的外周血声细胞已经被激活以表达更高密度的CD 14。此外，我们观察到在活动性RA中循环血液单核细胞亚群上C 014密度增加，HLA-DR没有显著改变，并且在活动性和非活动性RA中Fc γ RI和Fc γ RI 1增加，这与IFN-γ的预期作用不一致。最后，表明RA患者外周血单核细胞可能具有内在异常，如Fc γ R表达增强所证明的，这是与RA的疾病活动无关的特异性观察。类风湿性关节炎（RA）的发生与遗传和环境因素有关。我们描述了一个病人谁开发的进展性RA后输血相关的丙型肝炎病毒感染离子。有趣的是，我们的患者具有HLA-DR 4和HLA-Bw 54的组合，这在日本RA患者中经常观察到，表明他对该疾病具有遗传易感性。这表明，丙型肝炎病毒可能会引发遗传易感个体的RA的发展。当然，应该指出的是，RA可能是我们患者的偶然事件。对RA合并丙型肝炎病毒感染的患者应进行前瞻性研究，在关节液、关节组织或其他部位寻找证据，以区分RA是否由丙型肝炎病毒感染引发，或者丙型肝炎病毒本身是否存在于关节中，引起免疫复合物反应或直接细胞毒性。少

Synovial fluids(SF)and sera(S)from patients witn rheumatoid arthritis(RA)were examined for IgM, IgM-rheumatoid factor(IgM-RF). albumin in and interleukin-6(IL-6)activity. The quotient of SFIS IGN-RF was elevated compared with that of SF/S albumin in 7 patients with seropositiye RA, although the quotient of SF/S IgN was low er than that of SF/S albumin. SF IL-6 activity was much higher than serum IL-6 activity in all the 7 RA patients. In synovial fluids from 22 seropositiye RA patients, SF IL-6 activity was significantly correlated with the SF I gill-RF. IGG-RF and IGA-RF, but not with SF[gM, [gG or IgA. Moreover, SF IGM-RF as well as SF IL-6 activity was significantly correlated with the Westergren erythrocyte sedimentation rate(ESR)or the Lansbury articular index. These results indicate that(L-6and RF might be Produced within the rheumatoid joints as a result of abnormal im mune system activation, which is associated with the disease activity of RA. Three of the 4 seronegative RA pat … More ients, however, showed high SF IL-6 without detectable levels of SF IGM-RF. indicating that IL-6 alone is not sufficient for IGM-RF production.The expression of CD14, Fc gamma receptor l(FcgammaRI), FcrRH, and HLA-DR on peripheral blood monocutes from 9 atients with rheumatoid arthritis(RA)was studied to investigate their natures and their roles i. 1 the pathogenes is of rheumatoid synovitis. Peripheral blood mononuclear cells obtained from 9 patients with active RA, 8 patien ts with RA in complete remission, and 14 healthy individuals, were stained with various monoclonal antibodies and analyzed on fluourescence activated cell sorter. The expression of CD14 as well as FcgammaRI and FcgammaRII was upregu lated on peripheral blood monocutes from active RA patients, although the expression of HLA-DR was not increased. In addition, the expression of FcgammaRI and FcRII on monocutes was still upregulated in RA patients in complete remi ssion, whereas the expression of CD14 on sonocytes was normalized in these patients. These results indicate that Peripheral blood sonocytes in active RA patients are already activated to express higher densities of CD14. In ad dition, our observation that C014 density was increased on a subset of circulating blood monocutes in active RA, that HLA-DR was not significantly altered and that FcgammaRI and FcgammaRIl were increased in both active and inactive RA is not compatible with the expected actions of IFN-gamma. Finally, it is suggested that peripheral blood monocut es in RA patients may have intrinsic abnormalities as evidenced by the enhanced expression of FcgammaRs, which is pe rsistently observed irrespective of the disease activity of RA. The development of rheumatoid arthritis(RA)has been considered to involve both genetic and environmental f actors. We describe a patient who developed Progressive RA after transfusion-associated hepatitis C virus infect ion. Of interest, our patient possessed the combination of HLA-DR4 and HLA-Bw54, which has been frequently observe d in Japanese patients with RA, indicating that he was genetically susceptible to the disease. This suggests that hepatitis C virus may trigger the development of RA in genetically susceptible individuals. It should of course be pointed out that RA could have been a chance occurrence in our patient. Patients with RA and hepatitis C virus infection should be studied prospectively to seek evidence in the joint fluid, joint tissue, or elsewhere, to distinguish whether the RA is triggered by hepatitis C infection or whether hepatitis C virus itself resides in th e joint, causing either an immune complex reaction or direct cytotoxicity. Less