摘要
In the last decade,substantial progress has been made in understanding the molecular mechanisms involved in the initial host responses to viral infections.Herpes-viral infections can provoke an inflammatory cytokine response,however,the innate pathogen-sensing mechanisms that transduce the signal for this response are poorly understood.In recent years,it has become increasingly evident that the Toll-like receptors(TLRs),which are germline-encoded pattern recognition re-ceptors(PRRs),function as potent sensors for infection.TLRs can induce the activation of the innate immunity by recruiting specific intracellular adaptor proteins to initiate signaling pathways,which then culminating in activation of the nuclear factor kappa B(NF-κB)and interferon-regulatory factors(IRFs)that control the transcription of genes encoding type I interferon(IFN I)and other inflammatory cytokines.Furthermore,activa-tion of innate immunity is critical for mounting adaptive immune responses.In parallel,common mechanisms used by viruses to counteract TLR-mediated responses or to actively subvert these pathways that block recog-nition and signaling through TLRs for their own benefit are emerging.Recent findings have demonstrated that TLR2 plays a crucial role in initiating the inflammatory process,and surprisingly that the response TLR2 trig-gers might be overzealous in its attempt to counter the attack by the virus.In this review,we summarize and discuss the recent advances about the specific role of TLR2 in triggering inflammatory responses in herpes-virus infection and the consequences of the alarms raised in the host that they are assigned to protect.
基金
supported by grants from the National Basic Research Program(973 Program)(Nos.2010CB530105 and 2011CB504802)
the Start-up Fund of the Hundred Talents Program of the Chinese Academy of Sciences(No.20071010-141)
the National Natural Science Foundation of China(Grant No.30870120).
作者简介
Correspondence:Chun-fu Zheng,zheng.alan@hotmail.com;Ming-sheng Cai,contributed equally to the work;Mei-li Li,contributed equally to the work。
