Singh A K
Tufts-New England Medical Center, Boston.
J R Coll Physicians Lond. 1992 Oct;26(4):374-6.
Excessive production of pathogenic autoantibodies is one of the hallmarks of systemic lupus erythematosus (SLE). The mechanisms that underlie this excessive production are still unclear. Although there is considerable evidence to suggest that both T-cells and B-cells play an important role in the aetiology of SLE, convincing abnormalities at the T-cell receptor or immunoglobulin gene loci have not been demonstrated. In this regard, because cytokines play a pivotal role in the inflammatory response, a defect in the immunoregulation of B-cells by cytokines should be considered as a potential contender in disease aetiology. The hypothesis proposed here is that multiple cytokine-mediated defects are present in individuals with lupus and that both cytokine production and the response of B-cells to cytokines may be defective.
致病性自身抗体的过度产生是系统性红斑狼疮(SLE)的标志性特征之一。这种过度产生的潜在机制仍不清楚。尽管有大量证据表明T细胞和B细胞在SLE的病因中都起着重要作用,但尚未在T细胞受体或免疫球蛋白基因位点发现令人信服的异常。在这方面,由于细胞因子在炎症反应中起关键作用,细胞因子对B细胞免疫调节的缺陷应被视为疾病病因中的一个潜在因素。这里提出的假设是,狼疮患者存在多种细胞因子介导的缺陷,细胞因子的产生以及B细胞对细胞因子的反应可能都存在缺陷。