Littman B H, Schwartz P
Arthritis Rheum. 1982 Mar;25(3):288-96. doi: 10.1002/art.1780250306.
The ability of gold sodium thiomalate to inhibit production of the second complement component (C2) by monocytes stimulated by a lymphokine (monocyte complement stimulator is demonstrated. This gold salt inhibits C2 production irreversibly if monocytes are incubated with it before or during lymphokine stimulation. Thiomalic acid is not inhibitory. Monocytes already stimulated by lymphokine are resistant to inhibition of C2 production by gold sodium thiomalate. Gold salts do not reduce monocyte viability, phagocytic ability (latex heads) accessory cell function (as measured by the ability to present antigen to autologous lymphocytes), or capacity to act as stimulating cells in mixed leukocyte culture. Gold sodium thiomalate's inhibition of monocyte responsiveness to lymphokine may be significant in explaining the therapeutic benefit of gold salts in rheumatoid arthritis.
已证实硫代苹果酸钠金抑制淋巴细胞因子刺激的单核细胞产生第二补体成分(C2)的能力(单核细胞补体刺激物)。如果在淋巴细胞因子刺激之前或期间将单核细胞与该金盐一起孵育,这种金盐会不可逆地抑制C2的产生。硫代苹果酸没有抑制作用。已经受到淋巴细胞因子刺激的单核细胞对硫代苹果酸钠金抑制C2产生具有抗性。金盐不会降低单核细胞的活力、吞噬能力(乳胶颗粒)、辅助细胞功能(通过向自体淋巴细胞呈递抗原的能力来衡量)或在混合白细胞培养中作为刺激细胞的能力。硫代苹果酸钠金对单核细胞对淋巴细胞因子反应性的抑制作用可能在解释金盐在类风湿性关节炎中的治疗益处方面具有重要意义。