LEISHMANIASIS IN BEIGE MICE
LEISHMANIASIS IN BEIGE MICE
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DOI：
10.1128/iai.38.3.1208-1216.1982
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发表时间：
1982-01-01
影响因子：
3.1
通讯作者：
FARRELL, JP
中科院分区：
文献类型：
--
作者：
KIRKPATRICK, CE;FARRELL, JP
在3组C57BL/6J小鼠中研究了两种原虫病——皮肤利什曼病和内脏利什曼病的病程。一组小鼠为米色基因纯合隐性（bg/bg）。米色小鼠是人类切迪阿克 - 东综合征的遗传同源物，除其他缺陷外，其天然杀伤细胞活性严重缺乏。野生型（+/+）小鼠通过最终清除寄生虫对实验性皮肤或内脏利什曼病产生反应，杂合米色（bg/+）小鼠作为对照；两者在天然杀伤细胞活性方面表型正常，脾脏中的天然杀伤细胞活性尤其高。在bg/bg小鼠中，皮肤利什曼病的病原体热带利什曼原虫在初次接种和激发接种后的病程与对照小鼠相似。所有组的小鼠对热带利什曼原虫抗原都表现出相似的体液和细胞免疫反应。与bg/+和+/+对照小鼠不同，在内脏利什曼病的病原体杜氏利什曼原虫的无鞭毛体在56天的观察期内未从bg/bg小鼠的脾脏中被清除。所有组的小鼠都产生了相似水平的抗利什曼原虫抗体，并且所有小鼠对杜氏利什曼原虫抗原的足垫注射都有相似的反应。研究表明天然杀伤细胞在从杜氏利什曼原虫感染恢复中可能起作用，但在从热带利什曼原虫感染恢复中不起作用。
The courses of 2 protozoal diseases, cutaneous and visceral leishmaniasis, were examined in 3 gruops of C57BL/6J mice. One group of mice was homozygous recessive for the beige gene (bg/bg). Beige mice are the genetic homologue of the human Chediak-Higashi syndrome and, among other defects, are profoundly deficient in natural killer cell activity. Wild-type (+/+) mice, which resond to experimental cutaneous or visceral leishmaniasis by eventually eliminating their parasites, and heterozygous beige (bg/+) mice served as controls; both are phenotypically normal in natural killer cell activity, which is particularly high in the spleen. In bg/bg mice, the course of Leishmania tropica, a causative agent of cutaneous leishmaniasis, was similar to that in control mice after both primary and challenge inoculations. All groups of mice expressed similar humoral and cellular immune responses to L. tropica antigen. Amastigotes of L. donovani, a causative agent of visceral leishmaniasis, were not eliminated from the spleens of bg/bg mice over an observation period of 56 days, in contrast to bg/+ and +/+ controls. Similar levels of anti-leishmanial antibody were produced by all groups of mice, and all mice responded comparably to footpad injections of L. donovani antigen. A possible role for natural killer cells in recovery from L. donovani but not from L. tropica infection was suggested.