Singh A K
Division of Nephrology, Tufts-New England Medical Center, Boston, Massachusetts 02111.
Med Hypotheses. 1992 Dec;39(4):356-9. doi: 10.1016/0306-9877(92)90061-g.
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 etiology of SLE, convincing abnormalities at the T cell receptor or immunoglobulin gene loci have not been demonstrated. In this regard, because cytokines play such a pivotal role in the inflammatory response, a defect in the immunoregulation of B cells by cytokines should be considered as possible contender in disease etiology. The hypothesis that is proposed here is that multiple defects mediated by cytokines are present in individuals with lupus and that both cytokine production and the response of B cells to cytokines may be defective. These abnormalities could then be a central factor in the etiology of systemic lupus erythematosus.
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。导致这种过度产生的机制仍不清楚。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，但尚未证实T细胞受体或免疫球蛋白基因位点存在令人信服的异常。在这方面，由于细胞因子在炎症反应中起着关键作用，细胞因子对B细胞的免疫调节缺陷应被视为疾病病因的一个可能因素。这里提出的假说是，狼疮患者存在由细胞因子介导的多种缺陷，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。这些异常可能是系统性红斑狼疮病因的核心因素。
