Immunoregulatory aberrations in systemic lupus erythematosus.
Immunoregulatory aberrations in systemic lupus erythematosus.
复制标题
系统性红斑狼疮的免疫调节异常。
作者：
A. Fauci;A. Steinberg;B. Haynes;G. Whalen
本研究旨在探讨系统性红斑狼疮（SLE）患者免疫调节缺陷的性质。38例SLE患者除T淋巴细胞绝对减少外，还存在IgG（TG）受体T细胞亚群的选择性比例和数量缺陷（P < 0.01）。该T细胞亚群先前已被证明是美洲商陆有丝分裂原（PWM）驱动的胞质内IG产生中的抑制细胞群。具有IgM（TM）受体的T细胞已被证明是产生IG的辅助性T细胞，在比例或绝对数量上与正常人没有显著差异。
用PWM诱导的空斑形成细胞（PFC）对绵羊红细胞（SRBC）的反应，SLE患者为18（±4.2）PFC/106淋巴细胞，明显低于正常人的153（±18.4）PFC/106淋巴细胞（P < 0.001）。这种被抑制的PFC反应被认为是由于体内多克隆激活与自身免疫状态。
SLE患者有一个显着的缺陷，他们的淋巴细胞的能力后，刀豆蛋白A激活产生抑制细胞的PWM诱导的PFC反应，而他们的能力受到抑制的抑制刺激似乎完好无损。尽管患者之间存在相当大的差异，但SLE患者的淋巴细胞一般具有足够的T辅助细胞功能，并且可以得到正常同种异体T辅助细胞的帮助。因此，这项研究表明，SLE患者有一个数量缺陷的T细胞亚群与抑制能力。此外，它们在适当激活后产生抑制细胞功能的能力方面存在缺陷。这些发现可能有助于进一步了解SLE的免疫调节缺陷。
This study was undertaken to delineate the nature of the immunoregulatory defect in patients with systemic lupus erythematosus (SLE). Thirty-eight SLE patients were studied and it was found that in addition to an absolute T lymphocytopenia, these patients had a selective proportional and quantitative deficiency (P < 0.01) of a subpopulation of T cells possessing a receptor for IgG (TG). This T cell subpopulation has been previously demonstrated to be the suppressor cell population in pokeweed mitogen (PWM)-driven intracytoplasmic Ig production. T cells with a receptor for IgM (TM) which have been shown to be the helper T cells for Ig production were not significantly different from normals in proportion or absolute numbers.
By employing a PWM-induced plaque-forming cell (PFC) assay against sheep red blood cells (SRBC), it was shown that SLE patients had a markedly reduced response of 18 (±4.2) PFC/106 lymphocytes compared to normals with 153 (±18.4) PFC/106 lymphocytes (P < 0.001). This suppressed PFC response was felt to result from in vivo polyclonal activation associated with the autoimmune state.
SLE patients had a marked defect in the ability of their lymphocytes after Con A activation to generate suppressor cells of the PWM-induced PFC response, whereas their ability to be suppressed by suppressor stimuli appeared intact. Despite considerable variability from patient to patient, lymphocytes from SLE patients in general had adequate T helper cell function and could be helped by normal allogeneic T helper cells. Thus, this study demonstrates that SLE patients have a quantitative defect in a subpopulation of T cells with suppressor capability. In addition, they have a defect in the ability to generate suppressor cell function upon appropriate activation. These findings may lend further insight into the understanding of the immunoregulatory defect in SLE.