Pan L Z, Dauphinée M J, Ansar Ahmed S, Talal N
Scand J Immunol. 1986 Apr;23(4):415-23. doi: 10.1111/j.1365-3083.1986.tb03073.x.
Three strains of mice bearing the autosomal recessive lpr gene (MRL, C57BL/6, and C3H) that had spontaneously developed a lupus-like disease were studied sequentially for functional natural killer (NK) and natural cytotoxic (NC) cell activity. Natural killing was impaired in spleen and bone marrow cells from all the lpr strains, as well as from the congenic strain MRL--+/+, which develops a late onset lupus-like disease. The NK cell activity was found to be depleted as early as 2 months of age in all lpr strains, and decreased further with age. NK activity was augmentable by Poly I:C and interleukin 2 (IL-2), suggesting that the residual cells can respond to NK modulators. In contrast with NK cell activity, NC activity was not decreased in lpr mice but could be augmented by IL-3-rich supernatants. The spontaneous decrease in NK cell activity was associated with an increased autologous plaque-forming cell (APFC) response to bromelin-treated mouse red blood cells, which is produced primarily by B cells possessing the Ly-1 phenotype (Lyt-1+ B). When NK cell activity was increased by exogenous administration of Poly I:C, the APFC response diminished. Treatment of spleen cells with anti-asialo GM1 prior to Poly I:C treatment resulted in a decreased NK response but increased both APFC and Lyt-1+ B cells. The possible regulation of autoreactivity by NK cells is discussed.
对三种携带常染色体隐性lpr基因的小鼠品系（MRL、C57BL/6和C3H）进行了研究，这些品系已自发发展出狼疮样疾病，依次检测其功能性自然杀伤（NK）细胞和自然细胞毒性（NC）细胞活性。所有lpr品系以及同基因品系MRL--+/+（其会发展出迟发性狼疮样疾病）的脾脏和骨髓细胞中的自然杀伤功能均受损。在所有lpr品系中，早在2月龄时就发现NK细胞活性降低，并随年龄进一步下降。NK活性可被聚肌胞苷酸（Poly I:C）和白细胞介素2（IL-2）增强，这表明残余细胞能够对NK调节剂作出反应。与NK细胞活性相反，lpr小鼠的NC活性并未降低，但富含IL-3的上清液可增强其活性。NK细胞活性的自发降低与对菠萝蛋白酶处理的小鼠红细胞的自体空斑形成细胞（APFC）反应增加有关，该反应主要由具有Ly-1表型（Lyt-1+ B）的B细胞产生。当通过外源性给予Poly I:C增加NK细胞活性时，APFC反应减弱。在给予Poly I:C之前用抗唾液酸GM1处理脾细胞会导致NK反应降低，但APFC和Lyt-1+ B细胞均增加。本文讨论了NK细胞对自身反应性的可能调节作用。
