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Interleukin-2 reverses deficient cell-mediated immune responses in rheumatoid arthritis.

机译:白细胞介素2逆转类风湿关节炎中不足的细胞介导的免疫反应。

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摘要

The depressed cell-mediated immunity in rheumatoid arthritis was investigated in vivo by cutaneous hypersensitivity responses to seven antigens including tuberculin PPD, and in vitro by lymphocyte transformation to the latter antigen. In vivo 40% of rheumatoid patients were anergic compared to 2% of controls (P less than 0.001) with an associated reduction in sum score (5.9 +/- 6.5 vs 15.3 +/- 8.7, P less than 0.001). In vitro lymphocyte proliferation to PPD was also significantly depressed (P less than 0.001) and could not be reversed by indomethacin. A significant correlation between the in vivo sum scored (induration in mm) and in vitro thymidine incorporation (d/min) (r = 0.59, P less than 0.001) was found. In an attempt to overcome the depressed in vitro response the addition of a crude supernatant from a mixed lymphocyte reaction was found to return the PPD stimulated lymphocyte proliferation to the normal range. This effect was mimicked by purified IL-2 but not purified IL-1. The implications of this finding are are discussed.
机译:通过对包括结核菌素PPD在内的7种抗原的皮肤超敏反应,在体内研究了类风湿性关节炎中抑制的细胞介导的免疫,并通过对后者抗原的淋巴细胞转化在体外进行了研究。体内有40%的类风湿病患者是无反应的,而对照组则为2%(P小于0.001),总得分降低(5.9 +/- 6.5对15.3 +/- 8.7,P小于0.001)。体外淋巴细胞向PPD的增殖也被显着抑制(P小于0.001),并且吲哚美辛无法逆转。发现体内总分(以毫米为单位)和体外胸苷掺入(d / min)之间存在显着相关性(r = 0.59,P小于0.001)。为了克服体外反应低下的现象,发现从混合淋巴细胞反应中加入粗上清液可使PPD刺激的淋巴细胞增殖恢复到正常范围。纯化的IL-2模仿了这种效果,但纯化的IL-1却没有。讨论了这一发现的含义。

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