Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus.
Intracellular Sequestration of the NKG2D Ligand MIC B by Species F Adenovirus.
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DOI：
10.3390/v13071289
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发表时间：
2021-07-01
期刊：
影响因子：
--
通讯作者：
Bouvier M
中科院分区：
文献类型：
--
作者：
Oliveira ERA;Li L;Bouvier M
包括HAdV-F40和HAdV-F41的F种肠道人腺病毒（HAdVs-F）是引起全世界儿童急性胃肠炎的重要病原体。HAdVs-F的早期转录单位3（E3）与其他HAdV种的E3有显著不同。迄今为止，HAdVs-F特有的E3蛋白尚未被表征，并且HAdVs-F逃避胃肠道（GI）中的免疫防御的机制知之甚少。在这里，我们表明，HAdV-F41感染的人肠HCT 116细胞上调表达的MHC I类相关链A（MIC A）和MIC B相对于未感染的细胞。我们的结果还表明，对于MIC B，这种反应并没有导致细胞表面上MIC B的显著增加。相反，MIC B大部分被隔离在细胞内。因此，尽管HAdV-F41感染HCT 116细胞上调MIC B表达，但配体仍保留在感染细胞内。在这些细胞中不能对MIC A进行类似的观察。我们的初步发现代表了HAdVs-F的一种新功能，可能使这些病毒能够逃避感染肠道中自然杀伤（NK）细胞的免疫监视，从而为未来研究其独特的E3蛋白铺平了道路。
The enteric human adenoviruses of species F (HAdVs-F), which comprise HAdV-F40 and HAdV-F41, are significant pathogens that cause acute gastroenteritis in children worldwide. The early transcription unit 3 (E3) of HAdVs-F is markedly different from that of all other HAdV species. To date, the E3 proteins unique to HAdVs-F have not been characterized and the mechanism by which HAdVs-F evade immune defenses in the gastrointestinal (GI) tract is poorly understood. Here, we show that HAdV-F41 infection of human intestinal HCT116 cells upregulated the expression of MHC class I-related chain A (MIC A) and MIC B relative to uninfected cells. Our results also showed that, for MIC B, this response did not however result in a significant increase of MIC B on the cell surface. Instead, MIC B was largely sequestered intracellularly. Thus, although HAdV-F41 infection of HCT116 cells upregulated MIC B expression, the ligand remained inside infected cells. A similar observation could not be made for MIC A in these cells. Our preliminary findings represent a novel function of HAdVs-F that may enable these viruses to evade immune surveillance by natural killer (NK) cells in the infected gut, thereby paving the way for the future investigation of their unique E3 proteins.
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