Toll-like receptor 3(TLR3)is a member of the TLR family,mediating the transcriptional induction of type I interferons(IFNs),proinflammatory cytokines,and chemokines,thereby collectively establishing an antiviral host ...Toll-like receptor 3(TLR3)is a member of the TLR family,mediating the transcriptional induction of type I interferons(IFNs),proinflammatory cytokines,and chemokines,thereby collectively establishing an antiviral host response.Studies have shown that unlike other TLR family members,TLR3 is the only RNA sensor that is utterly dependent on the Tollinterleukin-1 receptor(TIR)-domain-containing adaptor-inducing IFN-β(TRIF).However,the details of how the TLR3-TRIF signaling pathway works in an antiviral response and how it is regulated are unclear.In this review,we focus on recent advances in understanding the antiviral mechanism of the TRIF pathway and describe the essential characteristics of TLR3 and its antiviral effects.Advancing our understanding of TLR3 may contribute to disease diagnosis and could foster the development of novel treatments for viral diseases.展开更多
HEp-2 cells persistently infected with respiratory syncytial virus(RSV) are a heterogeneous mixture of viral antigen-positive and-negative variants; however, the mechanism through which viral replication becomes laten...HEp-2 cells persistently infected with respiratory syncytial virus(RSV) are a heterogeneous mixture of viral antigen-positive and-negative variants; however, the mechanism through which viral replication becomes latent remains unclear. In this study, we investigated the potential mechanism by which RSV escapes from innate immune surveillance. Persistent-infected RSV HEp-2 cells were isolated and cell clones were passaged. The RSV-persistent cells produced viruses at a lower titer, resisted wild-type RSV re-infection, and secreted high levels of interferon-β(IFN-β), macrophage inflammatory protein-1α(Mip-1α), interleukin-8(IL-8), and Rantes. Toll-like receptor 3(TLR3), retinoic acid inducible gene-I(RIG-I), and suppressor of cytokine signaling 1(SOCS1) levels were upregulated in these cells. The silencing of TLR3 m RNA decreased the expression of SOCS1 protein and the secretion of cytokines. RSV-persistent cells are in an inflammatory state; upregulation of SOCS1 is related to the TLR3 signaling pathway, which could be associated with the mechanism of viral persistence.展开更多
基金supported by the National Key R&D Program of China(No.2018YFD0501705)the Chongqing Basic Research Program(No.cstc2018jcyj AX0615)the Fundamental Research Funds for the Central Universities(Nos.XDJK2018C059 and XDJK2018C060),China。
文摘Toll-like receptor 3(TLR3)is a member of the TLR family,mediating the transcriptional induction of type I interferons(IFNs),proinflammatory cytokines,and chemokines,thereby collectively establishing an antiviral host response.Studies have shown that unlike other TLR family members,TLR3 is the only RNA sensor that is utterly dependent on the Tollinterleukin-1 receptor(TIR)-domain-containing adaptor-inducing IFN-β(TRIF).However,the details of how the TLR3-TRIF signaling pathway works in an antiviral response and how it is regulated are unclear.In this review,we focus on recent advances in understanding the antiviral mechanism of the TRIF pathway and describe the essential characteristics of TLR3 and its antiviral effects.Advancing our understanding of TLR3 may contribute to disease diagnosis and could foster the development of novel treatments for viral diseases.
基金supported by the National Natural Science Foundation of China (No. 81170005 and No. 30973220)
文摘HEp-2 cells persistently infected with respiratory syncytial virus(RSV) are a heterogeneous mixture of viral antigen-positive and-negative variants; however, the mechanism through which viral replication becomes latent remains unclear. In this study, we investigated the potential mechanism by which RSV escapes from innate immune surveillance. Persistent-infected RSV HEp-2 cells were isolated and cell clones were passaged. The RSV-persistent cells produced viruses at a lower titer, resisted wild-type RSV re-infection, and secreted high levels of interferon-β(IFN-β), macrophage inflammatory protein-1α(Mip-1α), interleukin-8(IL-8), and Rantes. Toll-like receptor 3(TLR3), retinoic acid inducible gene-I(RIG-I), and suppressor of cytokine signaling 1(SOCS1) levels were upregulated in these cells. The silencing of TLR3 m RNA decreased the expression of SOCS1 protein and the secretion of cytokines. RSV-persistent cells are in an inflammatory state; upregulation of SOCS1 is related to the TLR3 signaling pathway, which could be associated with the mechanism of viral persistence.
