Differential Regulation of TLR Signaling on the Induction of Antiviral Interferons in Human Intestinal Epithelial Cells Infected with Enterovirus 71

作者：Wang, Chunyang; Ji, Lianfu; Yuan, Xinhui; Jin, Yu^*; Cardona, Carol J.; Xing, Zheng^*

来源：PLos One, 2016, 11(3): e0152177.

DOI：10.1371/journal.pone.0152177

• TOLL-LIKE RECEPTOR-3
• INDUCIBLE GENE-I
• NF-KAPPA-B
• INNATE IMMUNITY
• VIRAL REPLICATION
• RESPONSES
• PROTEIN
• MICE
• RECOGNITION
• ACTIVATION

Enterovirus 71 (EV71) causes hand-foot-and-mouth disease, which can lead to fatal neurological complications in young children and infants. Few gastrointestinal symptoms are observed clinically, suggesting the presence of a unique immunity to EV71 in the gut. We reported a robust induction of interferons (IFNs) in human intestinal epithelial cells (HT-29), which was suppressed in other types such as RD and HeLa cells. The underlying mechanism for the apparent difference remains obscure. In this study we report that in EV71-infected HT-29 cells, TLR/TRIF signaling was essential to IFN induction; viral replication increased and the induction of IFN-alpha, -beta, -omega, -kappa, and -epsilon decreased markedly in TRIF-silenced HT-29 cells. Importantly, TRIF was degraded by viral 3C(pro) in RD cells, but resisted cleavage, and IRF3 was activated and translocated into the nucleus in HT-29 cells. Taken together, our data suggest that IFNs were induced differentially in human HT-29 cells through an intact TLR/TRIF signaling, which differs from other cell types and may be implicated in viral pathogenesis in EV71 infection.

• 出版日期2016-3-23
• 单位南京医科大学; 南京大学