IMMUNE ABNORMALITIES IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

系统性红斑狼疮患者产生的B细胞数量增加 抗体，包括自身抗体。T细胞负责调节 B细胞产生抗体包括辅助细胞、抑制因子 细胞，并对每个细胞进行诱导。系统性红斑狼疮患者 抑制诱导细胞的数量和百分比 在功能上和由表型为CD+的细胞所测量的， 2H4+。这种异常在以下患者中尤其常见 活动性疾病和患有肾脏疾病的患者(尤其是有 疾病活动)。 系统性红斑狼疮患者被发现产生与 重组hnRNP核心蛋白A1。这样的抗体也被制造出来 一些幼年类风湿性关节炎患者。因为这个蛋白质结合了 核酸，它可以通过体内诱导抗DNA(反之亦然) 想象独一无二的机制。我们寻找，但找不到， 独特型诱导这种抗体的证据：抗DNA 而抗hnRNP核心蛋白A1抗体没有特殊的临时性 彼此之间的关系。日本血吸虫免疫小鼠的研究 重组hnRNP A1蛋白导致大量抗hnRNP 核心蛋白提示直接免疫可能是 在人体内诱导的机制。

Patients with SLE have increased numbers of B cells producing antibodies, including autoantibodies. T cells which regulate antibody production by B cells include helper cells, suppressor cells, and induces of each. Patients with SLE have a decrease in numbers and percentages of suppressor inducer cells both functionally and as measured by cells with the phenotype CD 4+, 2H4+. This abnormality is especially common in patients with active disease and in those with renal disease (especially with disease activity). Patient with SLE were found to produce antibodies reactive with recombinant hnRNP core protein A1. Such antibodies also were made by some patients with juvenile RA. Since this protein binds nucleic acids, it could induce anti-DNA (or vice versa) by internal image idiotypic mechanisms. We looked for, but could not find, evidence for an idiotypic induction of such antibodies: anti-DNA and anti-hnRNP core protein A1 antibodies bore no special temporal relationship with each other. Immunization of mice with recombinant hnRNP A1 protein led to large amounts of anti-hnRNP core protein suggesting that direct immunization might be the mechanism of induction in people.