感染伯氏疟原虫ANKA的小鼠中γδ T细胞功能在脑型疟疾发病机制中的作用
Gamma delta T-cell function in pathogenesis of cerebral malaria in mice infected with Plasmodium berghei ANKA.
作者信息
Yañez D M, Batchelder J, van der Heyde H C, Manning D D, Weidanz W P
机构信息
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison 53706, USA.
出版信息
Infect Immun. 1999 Jan;67(1):446-8. doi: 10.1128/IAI.67.1.446-448.1999.
Abstract
Mice depleted of gammadelta T cells by monoclonal antibody treatment and infected with Plasmodium berghei ANKA did not develop cerebral malaria (CM). In striking contrast, delta0/0 mice infected with P. berghei developed CM despite their gammadelta T-cell deficiency. gammadelta T cells appear to be essential for the pathogenesis of CM in mice having experienced normal ontogeny but not in mice genetically deprived of gammadelta T cells from the beginning of life.
摘要
通过单克隆抗体处理耗尽γδT细胞并感染伯氏疟原虫ANKA的小鼠未发生脑型疟疾（CM）。与之形成鲜明对比的是，感染伯氏疟原虫的δ0/0小鼠尽管存在γδT细胞缺陷，但仍发生了CM。γδT细胞似乎对于经历正常个体发育的小鼠的CM发病机制至关重要，但对于从生命开始就基因缺失γδT细胞的小鼠则并非如此。
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