Salkowski C A, Balish E
University of Wisconsin Medical School, Department of Surgery, Madison 53706.
J Leukoc Biol. 1991 Aug;50(2):151-9. doi: 10.1002/jlb.50.2.151.
These studies demonstrate that Cryptococcus neoformans infection induced a dose-dependent augmentation of splenic natural killer (NK) cell activity by bg/+, but not bg/bg mice. To directly assess the role of NK cells in resistance to C. neoformans, bg/+ and bg/bg mice were treated with anti-NK-1.1 monoclonal antibody (mAb). Anti-NK-1.1-treatment abrogated the augmented NK cell activity observed during C. neoformans infection in bg/+ mice. Anti-NK-1.1-treated bg/+ mice had higher C. neoformans colony forming units (CFU) in their lungs on days 3 and 7 after intravenous (i.v.) challenge than control bg/+ mice. Moreover, the number of C. neoformans CFU in the lungs of anti-NK-1.1-treated bg/+ mice on days 3 and 7 were similar to those observed for infected bg/bg mice. By day 14, however, no differences in C. neoformans CFU were evident in the lungs of anti-NK-1.1-treated and control bg/+ mice. Anti-NK-1.1-treatment did not alter either the growth of C. neoformans in the spleens, livers, kidneys, or brain of bg/+ mice or the susceptibility of bg/bg mice to systemic cryptococcosis. These studies suggest that NK cells do not play a role in resistance to systemic cryptococcosis in the spleen, but do appear to play an early, but transient role in resistance to C. neoformans in the lungs. Overall, congenital defects in polymorphonuclear neutrophils (PMNs) and macrophages (M phi s), in addition to defects in NK cells, contribute to the enhanced susceptibility of bg/bg mice to systemic cryptococcosis.
这些研究表明，新型隐球菌感染可使bg/+小鼠而非bg/bg小鼠的脾脏自然杀伤（NK）细胞活性呈剂量依赖性增强。为了直接评估NK细胞在抵抗新型隐球菌中的作用，对bg/+和bg/bg小鼠用抗NK-1.1单克隆抗体（mAb）进行处理。抗NK-1.1处理消除了在新型隐球菌感染期间bg/+小鼠中观察到的NK细胞活性增强。静脉内（i.v.）攻击后第3天和第7天，抗NK-1.1处理的bg/+小鼠肺部的新型隐球菌菌落形成单位（CFU）比对照bg/+小鼠更高。此外，抗NK-1.1处理的bg/+小鼠在第3天和第7天肺部的新型隐球菌CFU数量与感染的bg/bg小鼠中观察到的相似。然而，到第14天，抗NK-1.1处理的和对照bg/+小鼠肺部的新型隐球菌CFU没有明显差异。抗NK-1.1处理既未改变bg/+小鼠脾脏、肝脏、肾脏或大脑中新型隐球菌的生长，也未改变bg/bg小鼠对全身性隐球菌病的易感性。这些研究表明，NK细胞在抵抗脾脏中的全身性隐球菌病方面不起作用，但似乎在抵抗肺部新型隐球菌方面发挥早期但短暂的作用。总体而言，除了NK细胞缺陷外，多形核中性粒细胞（PMN）和巨噬细胞（M phi s）的先天性缺陷导致bg/bg小鼠对全身性隐球菌病的易感性增强。
