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| 1 | Herpesviral infection and Toll-like receptor 2显示文摘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. | Ming-sheng Cai Mei-li Li Chun-fu Zheng | 2012 | Protein & Cell2012，3，8： | 3 |
| 2 | Ubiquitination modification:critical regulation of IRF family stability and activity显示文摘Interferon regulatory factors(IRFs)play pivotal and critical roles in innate and adaptive immune responses;thus,precise and stringent regulation of the stability and activation of IRFs in physiological processes is necessary.The stability and activities of IRFs are directly or indirectly targeted by endogenous and exogenous proteins in an ubiquitin-dependent manner.However,few reviews have summarized how host E3 ligases/DUBs or viral proteins regulate IRF stability and activity.Additionally,with recent technological developments,details about the ubiquitination of IRFs have been continuously revealed.As knowledge of how these proteins function and interact with IRFs may facilitate a better understanding of the regulation of IRFs in immune responses or other biological processes,we summarized current studies on the direct ubiquitination of IRFs,with an emphasis on how these proteins interact with IRFs and affect their activities,which may provide exciting targets for drug development by regulating the functions of specific E3 ligases. | Bao-qin Liu Jin Jin Yi-yuan Li | 2021 | Science China(Life Sciences)2021，64，6： | 1 |
| 3 | 小鼠感染流感病毒后外周血IFN-α变化规律的研究显示文摘流感病毒是引起呼吸道疾病的主要病原体,侵袭机体的上皮细胞和中性粒细胞产生具有生物活性的细胞因子。通过抽取感染了普通流感病毒病人的血液对小鼠进行滴鼻感染实验,通过ELISA实验检测小鼠血清中细胞因子IFN-α的含量及其变化情况,阐明普通流感病毒对小鼠机体防御系统免疫激活过程中IFN-α的变化规律。实验结果显示,产生I型干扰素(IFN-α)随着时间的增加而变化,逐渐趋于平稳,为下一步研制新型通用流感疫苗奠定基础。 | 李艳 宁秋 韩德明 姚海虹 赵赫楠 赵丽辉 | 2015 | 长春理工大学学报(自然科学版)2015，38，3： | 0 |
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