抗SARS-COV-2感染的先天免疫应答机制

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引用次数: 0

摘要

冠状病毒(CoVs)的免疫发病机制仍在研究中。先天免疫成分可以区分自身和非自身抗原,参与病毒颗粒识别,并通过抗病毒蛋白的表达限制病毒复制。诱导针对冠状病毒的抗病毒先天免疫应答在很大程度上取决于模式识别受体(PRRs)对病原体相关分子模式分子(PAMPs)的识别。PAMPs激活(toll样受体)TLR级联并启动转录因子,包括核因子- κB (NF-Κb)、干扰素调节因子(IRF3)和(IRF7),从而合成干扰素(IFN)型Ⅰ。随后,Ⅰ型IFN抑制病毒复制,调节和调节免疫系统。树突状细胞(dc)存在于呼吸道。它们可以通过TLR识别病毒颗粒,启动先天和适应性免疫,并通过ifn的产生抑制病毒的传播。TLR损伤、IFN表达障碍和/或先天免疫反应不响应可能与病毒消除后的组织破坏有关。本文就SARS-COV-2非特异性免疫应答机制的研究进展进行综述。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mechanism of Innate Immune Responses Against SARS-COV-2 Infection
The immunopathogenesis of the Coronaviruses (CoVs) is still under study. The innate immunity components can differentiate self and non-self-antigens, be involved in viral particle recognition, and restrict viral replications through antiviral protein expressions. Induction of antiviral innate immune responses against CoV vastly depends on recognizing pathogen-associated molecular pattern molecules (PAMPs) by pattern recognition receptors (PRRs). PAMPs mount the activation of (Toll-Like Receptors) TLR cascade and initiate transcription factors, involving Nuclear Factor- κB (NF-Κb), Interferon Regulatory Factors (IRF3), and (IRF7), and this results in the synthesize of Interferons (IFN) type Ⅰ. Subsequently, type Ⅰ IFN inhibit viral replications, regulate and modulate the immune system. Dendritic cells (DCs) reside in the respiratory tracts. They can recognize viral particles via TLR and initiate innate and adaptive immunity and repress viral spreads through IFNs production. Impairment of TLR, impediment of IFN expression, and/or disresponse of innate immune responses may be associated with tissue destruction after viral elimination. Here, emerging the reviews knowledge on the mechanism of non-specific immune responses against SARS-COV-2.
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