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正常人和系统性红斑狼疮患者多克隆免疫球蛋白产生的同种异体抑制。

Allogeneic suppression of polyclonal immunoglobulin production in normals and patients with systemic lupus erythematosus.

作者信息

Clough J D, Krakauer R A, Frank S A, Calabrese L H

出版信息

Clin Exp Immunol. 1980 Oct;42(1):27-32.

Abstract

T lymphocytes suppressing in vitro polyclonal immunoglobulin production can be activated by allogeneic stimuli or concanavalin A (Con A). These cells are deficient in systemic lupus erythematosus (SLE). In order to investigate the cellular requirements for this effect, we studied IgM and IgG biosynthesis by (a) normal and SLE lymphocytes cultured with pokeweed mitogen (PWM) and mitomycin C-blocked allogeneic normal or SLE lymphocytes, and (b) by normal and irradiated lymphocytes cultured with PWM and with Con A-pretreated normal and irradiated allogeneic and autochthonous blocked lymphocytes. Results showed that blocked allogeneic normal cells or blocked Con A-pretreated, normal or irradiated, autochthonous or allogeneic cells served as potent stimuli for suppression of immunoglobulin biosynthesis by normal responder cells, but not by SLE responder cells. This suggests that Con A stimulates a radioresistant suppressor inducer cell which in turn activates a radiosensitive, proliferation-dependent suppressor effector cell; the latter can also be activated by allogeneic stimulation and is deficient in SLE.

摘要

抑制体外多克隆免疫球蛋白产生的T淋巴细胞可被同种异体刺激物或刀豆球蛋白A(Con A)激活。这些细胞在系统性红斑狼疮(SLE)中存在缺陷。为了研究产生这种效应的细胞需求,我们通过以下方式研究了IgM和IgG的生物合成:(a)将正常和SLE淋巴细胞与商陆有丝分裂原(PWM)以及丝裂霉素C处理的同种异体正常或SLE淋巴细胞共同培养;(b)将正常和经辐照的淋巴细胞与PWM以及经Con A预处理的正常和经辐照的同种异体及自体阻断淋巴细胞共同培养。结果显示,经阻断的同种异体正常细胞或经阻断的、经Con A预处理的正常或经辐照的自体或同种异体细胞可作为有效刺激物,抑制正常反应细胞的免疫球蛋白生物合成,但对SLE反应细胞无效。这表明Con A刺激了一种抗辐射的抑制诱导细胞,该细胞进而激活了一种对辐射敏感、依赖增殖的抑制效应细胞;后者也可被同种异体刺激激活,且在SLE中存在缺陷。

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本文引用的文献

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A simple chromatographic method for preparation of gamma globulin.
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Arthritis Rheum. 1980 Jan;23(1):24-9. doi: 10.1002/art.1780230105.
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Lancet. 1974 Sep 14;2(7881):609-13. doi: 10.1016/s0140-6736(74)91940-0.
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Clin Immunol Immunopathol. 1976 Sep;6(2):192-9. doi: 10.1016/0090-1229(76)90110-0.
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Arthritis Rheum. 1979 Jan;22(1):1-6. doi: 10.1002/art.1780220101.
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Cell Immunol. 1979 Jun;45(1):120-32. doi: 10.1016/0008-8749(79)90367-8.

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