SIVsmmPBj14 induces expression of a mucosal integrin on macaque lymphocytes.
SIVsmmPBj14 induces expression of a mucosal integrin on macaque lymphocytes.
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SIVsmmPBj14 诱导猕猴淋巴细胞上粘膜整合素的表达。
DOI：
10.1006/viro.1996.0010
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Dewhurst,S
中科院分区：
文献类型：
--
作者：
Gummuluru,S;Novembre,FJ;Seshi,B;Dewhurst,S
猴免疫缺陷病毒（SIVsmmPBj14）的PBj14分离物是一种急性致病性慢病毒，可引起猕猴严重的胃肠道疾病。本文报道的研究利用培养的猕猴淋巴细胞的流式细胞术分析和病毒感染猕猴组织标本的免疫组织化学染色，探讨了SIVsmmPBj14肠病表型的基础。数据显示，sivsmmpbj14的肠病性分子克隆诱导α e β7整合素的表达，这被认为介导t细胞的粘膜保留，而sivsmmpbj14的非肠病性衍生物的分子克隆则不这样做。因此，在急性sivsmmpbj14感染期间，α e - β7的表达升高可能是导致肠黏膜内异常大量t细胞积聚的原因，至少在一定程度上如此。
The PBj14 isolate of simian immunodeficiency virus, SIVsmmPBj14, is an acutely pathogenic lentivirus that causes severe gastrointestinal disease in macaque monkeys. The studies reported here examine the basis for the enteropathic phenotype of SIVsmmPBj14, using flow cytometric analysis of cultured macaque lymphocytes and immunohistochemical staining of tissue specimens from virus-infected macaques. The data show that enteropathic molecular clones of SIVsmmPBj14induce expression of the αEβ7integrin, which is believed to mediate mucosal retention of T-cells, whereas molecular clones from nonenteropathic derivatives of SIVsmmPBj14do not do so. Thus, elevated expression of αEβ7may be responsible, at least in part, for the accumulation of abnormally large numbers of T-cells within the intestinal mucosa during acute SIVsmmPBj14infection.