携带lpr基因的自身免疫小鼠中缺陷性迟发型超敏反应的分析
Analysis of defective delayed-type hypersensitivity in autoimmune mice bearing lpr gene.
作者信息
Okuyama H, Yamamoto K, Matsunaga T, Kobayashi S, Tashiro A
出版信息
Clin Exp Immunol. 1986 Jan;63(1):87-94.
Many functional defects of T-cells have been found in autoimmune prone, MRL/MpJ-lpr/lpr (MRL/lpr) mice. We examined the capacity of delayed-type hypersensitivity (DTH) induction and macrophage migration inhibition factor (MIF) production. MRL/lpr and C57BL/6J-lpr/lpr (B6/lpr) mice were tested for capacity of DTH by the footpad reaction to purified protein derivative of tuberculin (PPD) and lung granuloma formation after immunization with BCG-cell wall (BCGCW). In lpr mice, the ability to induce DTH against exogeneous antigenic stimulation decreased with age. The results show that the defect of DTH in lpr mice caused by deficiency of the MIF producing capacity of proliferated T-cells rather than suppressor cell activity for MIF production.
在自身免疫易感的MRL/MpJ-lpr/lpr（MRL/lpr）小鼠中发现了许多T细胞功能缺陷。我们检测了迟发型超敏反应（DTH）诱导能力和巨噬细胞移动抑制因子（MIF）产生情况。通过对结核菌素纯蛋白衍生物（PPD）的足垫反应以及用卡介苗细胞壁（BCGCW）免疫后肺肉芽肿形成情况，检测了MRL/lpr和C57BL/6J-lpr/lpr（B6/lpr）小鼠的DTH能力。在lpr小鼠中，针对外源性抗原刺激诱导DTH的能力随年龄下降。结果表明，lpr小鼠中DTH缺陷是由增殖T细胞产生MIF的能力缺乏所致，而非产生MIF的抑制细胞活性缺乏所致。
Zotero 插件