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类风湿关节炎中由于表面巯基(SH)氧化导致的单核细胞辅助功能缺陷。

Defective monocyte accessory function due to surface sulphydryl (SH) oxidation in rheumatoid arthritis.

作者信息

McKeown M J, Hall N D, Corvalan J R

出版信息

Clin Exp Immunol. 1984 Jun;56(3):607-13.

Abstract

Low serum sulphydryl (SH) levels are a feature of active rheumatoid arthritis (RA). We have investigated whether a similar blockade of membrane SH groups on mononuclear cells modifies the function of these cells in this disease. Using pokeweed mitogen stimulated IgG synthesis as the assay system, we have found that the accessory cell function of peripheral blood monocytes is totally dependent on free SH groups on the cell surface. Monocytes from patients with active RA display poor accessory cell function when compared with healthy monocytes or with cells from patients treated with D-penicillamine. The poor function of the rheumatoid accessory cells may be corrected in vitro by 2-mercaptoethanol (2-ME). Addition of 2-ME to the culture system also enhances IgG synthesis by rheumatoid mononuclear cells to normal levels. We suggest that surface SH-dependent mechanisms are responsible, at least in part, for the depressed mononuclear cell functions of rheumatoid cells in vitro and may explain some effects of D-penicillamine therapy in rheumatoid patients.

摘要

血清巯基(SH)水平低是活动性类风湿关节炎(RA)的一个特征。我们研究了单核细胞膜SH基团的类似阻断是否会改变这些细胞在该疾病中的功能。以商陆有丝分裂原刺激的IgG合成作为检测系统,我们发现外周血单核细胞的辅助细胞功能完全依赖于细胞表面的游离SH基团。与健康单核细胞或接受D-青霉胺治疗的患者的细胞相比,活动性RA患者的单核细胞显示出较差的辅助细胞功能。类风湿辅助细胞的功能缺陷在体外可被2-巯基乙醇(2-ME)纠正。向培养系统中添加2-ME也可将类风湿单核细胞的IgG合成提高到正常水平。我们认为,表面SH依赖性机制至少部分地导致了类风湿细胞在体外单核细胞功能的降低,并可能解释了D-青霉胺治疗类风湿患者的一些效果。

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