Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin.
Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin.
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DOI：
10.1038/ncomms6230
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发表时间：
2014-10-17
影响因子：
16.6
通讯作者：
Jensen, Liselotte E.
中科院分区：
文献类型：
--
作者：
Milora, Katelynn A.;Miller, Samantha L.;Sanmiguel, Julio C.;Jensen, Liselotte E.
单纯疱疹病毒-1（HSV-1）是一种人类病原体，它利用几种策略来规避宿主免疫反应。HSV-1采用的免疫逃避机制是白细胞介素-1 β（IL-1β）在细胞内空间中的保留，其阻断IL-1β的促炎活性。在这里，我们报道了HSV-1感染的角质形成细胞主动释放促炎性IL-1α，保持了感染细胞向周围组织发出危险信号的能力。IL-1α的细胞外释放不依赖于炎性caspase。白细胞在表皮内早期HSV-1微感染部位的体内募集依赖于IL-1信号传导。皮肤HSV-1感染后，不能通过细胞外IL-1α发出信号的小鼠表现出与病毒传播相关的死亡率增加。我们的结论是，IL-1α作为一个alarmin必不可少的白细胞募集和保护性免疫HSV-1。这种功能可能是为了抵消HSV-1部署的免疫逃避机制而进化的。
Herpes simplex virus-1 (HSV-1) is a human pathogen that utilizes several strategies to circumvent the host immune response. An immune evasion mechanism employed by HSV-1 is retention of interleukin-1β (IL-1β) in the intracellular space, which blocks the pro-inflammatory activity of IL-1β. Here, we report that HSV-1 infected keratinocytes actively release the also pro-inflammatory IL-1α, preserving the ability of infected cells to signal danger to the surrounding tissue. The extracellular release of IL-1α is independent of inflammatory caspases. In vivo recruitment of leukocytes to early HSV-1 micro-infection sites within the epidermis is dependent upon IL-1 signalling. Following cutaneous HSV-1 infection, mice unable to signal via extracellular IL-1α exhibit an increased mortality rate associated with viral dissemination. We conclude that IL-1α acts as an alarmin essential for leukocyte recruitment and protective immunity against HSV-1. This function may have evolved to counteract an immune evasion mechanism deployed by HSV-1.
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