Immunoglobulin A-induced shift of Epstein-Barr virus tissue tropism.
Immunoglobulin A-induced shift of Epstein-Barr virus tissue tropism.
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DOI：
10.1126/science.1312750
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发表时间：
1992-03
期刊：
影响因子：
56.9
通讯作者：
J. Sixbey;Q. Yao
中科院分区：
文献类型：
--
作者：
J. Sixbey;Q. Yao
EB 病毒 (EBV) 免疫球蛋白 A (IgA) 抗体的增加出现在鼻咽癌临床发病前数月至数年，并确定了中国南方常见的 EBV 相关上皮癌的高危人群。在人类 HT-29 上皮细胞系中，EBV 特异性聚合 IgA (pIgA) 促进了难治性上皮细胞的感染。当与 pIgA 结合时，EBV 通过分泌成分介导的 IgA 转运进入上皮细胞，但不再感染 B 淋巴细胞。这种免疫诱导的 EBV 组织向性转变为 EBV 在免疫宿主中的内源性传播提供了范例，从而预测了上皮的感染性后遗症。
Increased immunoglobulin A (IgA) antibodies to the Epstein-Barr virus (EBV) appear months to years before the clinical onset of nasopharyngeal carcinoma and define populations at high risk for this EBV-associated epithelial cancer common in south China. In the human HT-29 epithelial cell line, polymeric IgA (pIgA) specific for EBV promoted infection of the otherwise refractory epithelial cells. When bound to pIgA, EBV entered epithelial cells through secretory component-mediated IgA transport but no longer infected B lymphocytes. Such an immune-induced shift in EBV tissue tropism provides a paradigm for endogenous spread of EBV in the immune host that predicts infectious sequelae of epithelium.