Winfield J B
Clin Rheum Dis. 1985 Dec;11(3):523-49.
Patients with systemic lupus erythematosus frequently develop antilymphocyte antibodies as measured by complement-dependent cytotoxicity and immunofluorescence assays. Highest titres of both of the major IgM and IgG classes occur during phases of active disease, and their presence is associated with essentially the entire spectrum of immune system functional abnormalities in this disorder. While the full range of antibody specificities requires further clarification, antibodies to many discrete lymphocyte populations have been described, including B cells, T cells, and T cell subsets. Antibodies to T cell subsets are of special interest because of their relationship with subset depletion in vivo, and their capacity to reproduce, through effects on normal cells in vitro, the same types of immunoregulatory abnormalities characteristic of lymphocytes isolated from patients with SLE. Suppressor/inducer and suppressor/effector T cells appear to be the main targets in this regard. Antibodies specific for activated T lymphocytes exist as well, and this type has the unusual property of interfering with events operant in production of/response to interleukin-2, a critical step controlling the expansion of specifically-reactive T cells and the induction of other lymphokines. In addition to complement-mediated lysis and antibody-dependent cell-mediated cytotoxicity, anti-lymphocyte antibodies have the potential to influence immune system function by several non-cytotoxic mechanisms, including surface antigen modulation and ligand/receptor triggering. Despite the large amount of data which has been accumulated concerning the cell type specificity and functional effects of anti-lymphocyte antibodies in SLE, little is known about the nature of the surface membrane molecules with which they react. Application of cell cloning and molecular biology technology should rectify this deficiency in the near future. Although it is likely that antilymphocyte antibodies are of relevance to immune system pathophysiology in SLE, it remains to be determined whether these interesting antibodies reflect secondary events, or have some more fundamental significance.
通过补体依赖细胞毒性和免疫荧光测定法测量发现,系统性红斑狼疮患者经常产生抗淋巴细胞抗体。在疾病活动期,主要的IgM和IgG类抗体的滴度最高,并且它们的存在与该疾病中基本上整个免疫系统功能异常谱相关。虽然抗体特异性的完整范围需要进一步阐明,但已经描述了针对许多离散淋巴细胞群体的抗体,包括B细胞、T细胞和T细胞亚群。针对T细胞亚群的抗体特别受关注,因为它们与体内亚群耗竭有关,并且通过对体外正常细胞的作用,它们能够重现从SLE患者分离的淋巴细胞所特有的相同类型的免疫调节异常。在这方面,抑制/诱导性T细胞和抑制/效应性T细胞似乎是主要靶标。也存在对活化T淋巴细胞具有特异性的抗体,并且这种类型具有干扰白细胞介素-2产生/反应中起作用的事件的不寻常特性,白细胞介素-2是控制特异性反应性T细胞扩增和其他淋巴因子诱导的关键步骤。除了补体介导的裂解和抗体依赖的细胞介导的细胞毒性外,抗淋巴细胞抗体还可能通过几种非细胞毒性机制影响免疫系统功能,包括表面抗原调节和配体/受体触发。尽管已经积累了大量关于SLE中抗淋巴细胞抗体的细胞类型特异性和功能效应的数据,但对于它们与之反应的表面膜分子的性质知之甚少。细胞克隆和分子生物学技术的应用应在不久的将来纠正这一缺陷。虽然抗淋巴细胞抗体可能与SLE中的免疫系统病理生理学相关,但这些有趣的抗体是反映继发性事件还是具有更根本的意义仍有待确定。