Disease-promoting effects of type I interferons in viral, bacterial, and coinfections.
Disease-promoting effects of type I interferons in viral, bacterial, and coinfections.
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DOI：
10.1089/jir.2014.0227
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发表时间：
2015-04
期刊：
影响因子：
--
通讯作者：
Wack A
中科院分区：
文献类型：
--
作者：
Davidson S;Maini MK;Wack A
虽然I型干扰素（IFN）因其抗病毒和免疫刺激功能而被普遍认可，但越来越多的人认识到在病毒和细菌感染中不适当、过度或时机不当的I型IFN应答的有害影响。I型IFN促进易感性或严重性的潜在机制包括通过诱导细胞凋亡或抑制组织细胞增殖的直接组织损伤，由于过度炎症引起的免疫病理学，和由表达TRAIL和Fas的免疫细胞诱导的细胞死亡，以及通过IL-10、IL-27、PD-L1、IL-1Ra、以及拮抗IL-1、IL-12、IL-17、IFN-γ、KC和免疫应答的其它效应物的诱导或作用的其它调节分子。流感感染后的细菌重复感染是I型IFN可误导免疫应答的突出例子。这篇评论讨论了目前的信号强度，持续时间，时间，位置和细胞受体的参数，确定I型干扰素在感染中是否有有益或有害的影响的理解。
While type I interferons (IFNs) are universally acknowledged for their antiviral and immunostimulatory functions, there is increasing appreciation of the detrimental effects of inappropriate, excessive, or mistimed type I IFN responses in viral and bacterial infections. The underlying mechanisms by which type I IFNs promote susceptibility or severity include direct tissue damage by apoptosis induction or suppression of proliferation in tissue cells, immunopathology due to excessive inflammation, and cell death induced by TRAIL- and Fas-expressing immune cells, as well as immunosuppression through IL-10, IL-27, PD-L1, IL-1Ra, and other regulatory molecules that antagonize the induction or action of IL-1, IL-12, IL-17, IFN-γ, KC, and other effectors of the immune response. Bacterial superinfections following influenza infection are a prominent example of a situation where type I IFNs can misdirect the immune response. This review discusses current understanding of the parameters of signal strength, duration, timing, location, and cellular recipients that determine whether type I IFNs have beneficial or detrimental effects in infection.
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DOI：
10.1016/j.bbrc.2007.02.019
发表时间：
2007-04-13
影响因子：
3.1
作者：
Beilharz, Manfred W.;Cummins, Joseph M.;Bennett, Alayne L.
通讯作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
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作者：
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通讯作者：
Fuchs, Serge Y.
影响因子：
64.8
作者：
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