Kanda N, Tsuchida T, Tamaki K
Saitama Medical School, Japan.
Arthritis Rheum. 1999 Feb;42(2):328-37. doi: 10.1002/1529-0131(199902)42:2<328::AID-ANR16>3.0.CO;2-#.
To study the in vitro effect of estrogen on IgG anti-double-stranded DNA (anti-dsDNA) antibody and total IgG production in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE), in order to elucidate its regulatory role in SLE.
PBMC from SLE patients and normal donors were cultured with 17beta-estradiol (E2). IgG anti-dsDNA antibodies, total IgG, and cytokine activity in the culture supernatants were measured by enzyme-linked immunosorbent assay.
E2 enhanced production of IgG anti-dsDNA antibodies as well as total IgG in PBMC from SLE patients. Anti-dsDNA production in patients with inactive disease was less responsive to E2 than that in patients with active disease. E2 also enhanced total IgG, but not anti-dsDNA, production in the PBMC of normal donors. Antibody production was increased by E2 to a lesser extent in patients' B cells than in their PBMC. Anti-interleukin-10 (anti-IL-10) antibodies partially blocked the E2-induced increase in antibody production in patients' PBMC, but anti-IL-10 had no effect on B cells. E2 increased IL-10 production by patients' monocytes. Exogenous IL-10 acted additively with E2 in increasing antibody production in patients' B cells.
These results suggest that E2 may polyclonally increase the production of IgG, including IgG anti-dsDNA, in SLE patients' PBMC by enhancing B cell activity and by promoting IL-10 production in monocytes. These findings support the involvement of E2 in the pathogenesis of SLE.
研究雌激素对系统性红斑狼疮（SLE）患者外周血单个核细胞（PBMC）中IgG抗双链DNA（抗dsDNA）抗体及总IgG产生的体外作用，以阐明其在SLE中的调节作用。
将SLE患者和正常供者的PBMC与17β-雌二醇（E2）一起培养。通过酶联免疫吸附测定法检测培养上清液中的IgG抗dsDNA抗体、总IgG和细胞因子活性。
E2增强了SLE患者PBMC中IgG抗dsDNA抗体以及总IgG的产生。病情处于非活动期的患者中抗dsDNA的产生对E2的反应低于病情处于活动期的患者。E2还增强了正常供者PBMC中总IgG的产生，但未增强抗dsDNA的产生。患者B细胞中抗体产生受E2的影响程度低于其PBMC。抗白细胞介素10（抗IL-10）抗体部分阻断了E2诱导的患者PBMC中抗体产生的增加，但抗IL-10对B细胞无影响。E2增加了患者单核细胞IL-10的产生。外源性IL-10与E2在增加患者B细胞抗体产生方面具有相加作用。
这些结果表明，E2可能通过增强B细胞活性和促进单核细胞产生IL-10，多克隆地增加SLE患者PBMC中IgG（包括IgG抗dsDNA）的产生。这些发现支持E2参与SLE的发病机制。
