Matsumoto K
Second Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
Int Arch Allergy Appl Immunol. 1988;87(4):435-8. doi: 10.1159/000234715.
To investigate the role of cell-mediated immunity in the pathogenesis of experimental glomerulonephritis, we examined interleukin-1 (IL-1) activity in the culture supernatant of lipopolysaccharide-stimulated peritoneal macrophages from rats with an accelerated autologous form of nephrotoxic serum nephritis (NTSN). Modified NTSN was produced by an intravenous injection of nephrotoxic serum (NTS) into the rats which had previously been immunized with rabbit IgG and Freund's complete adjuvant. It was found that the NTSN rats had significantly increased levels of IL-1 activity when compared to the values obtained with normal controls and the other control group, consisting of pre-immunized rats (rabbit IgG), then given normal rabbit globulin instead of NTS. The administration of a rabbit anti-rat macrophage serum reduced the production of IL-1 activity in the NTSN rats. In this experimental model IL-1 synthesis by peritoneal macrophages is present early in the disease process and may be an important mediator of glomerular immune injury.
为研究细胞介导的免疫在实验性肾小球肾炎发病机制中的作用，我们检测了来自加速型自身免疫性肾毒性血清肾炎（NTSN）大鼠的脂多糖刺激的腹腔巨噬细胞培养上清液中的白细胞介素-1（IL-1）活性。改良的NTSN是通过向先前用兔IgG和弗氏完全佐剂免疫的大鼠静脉注射肾毒性血清（NTS）产生的。结果发现，与正常对照组和另一对照组（由预先免疫的大鼠（兔IgG）组成，然后给予正常兔球蛋白而非NTS）相比，NTSN大鼠的IL-1活性水平显著升高。给予兔抗大鼠巨噬细胞血清可降低NTSN大鼠IL-1活性的产生。在这个实验模型中，腹腔巨噬细胞合成IL-1在疾病过程早期就存在，并且可能是肾小球免疫损伤的重要介质。
