Z-DNA binding protein 1 orchestrates innate immunity and inflammatory cell death

IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Cytokine & Growth Factor Reviews Pub Date : 2024-06-01 DOI:10.1016/j.cytogfr.2024.03.005
Qixiang Song , Yuhang Fan , Huali Zhang , Nian Wang
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Abstract

Innate immunity is not only the first line of host defense against microbial infections but is also crucial for the host responses against a variety of noxious stimuli. Z-DNA binding protein 1 (ZBP1) is a cytosolic nucleic acid sensor that can induce inflammatory cell death in both immune and nonimmune cells upon sensing of incursive virus-derived Z-form nucleic acids and self-nucleic acids via its Zα domain. Mechanistically, aberrantly expressed or activated ZBP1 induced by pathogens or noxious stimuli enables recruitment of TANK binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3 to drive type I interferon (IFN-I) responses and activation of nuclear factor kappa B (NF-κB) signaling. Meanwhile, ZBP1 promotes the assembly of ZBP1- and absent in melanoma 2 (AIM2)-PANoptosome, which ultimately triggers PANoptosis through caspase 3-mediated apoptosis, mixed lineage kinase domain like pseudokinase (MLKL)-mediated necroptosis, and gasdermin D (GSDMD)-mediated pyroptosis. In response to damaged mitochondrial DNA, ZBP1 can interact with cyclic GMP-AMP synthase to augment IFN-I responses but inhibits toll like receptor 9-mediated inflammatory responses. This review summarizes the structure and expression pattern of ZBP1, discusses its roles in human diseases through immune-dependent (e.g., the production of IFN-I and pro-inflammatory cytokines) and -independent (e.g., the activation of cell death) functions, and highlights the attractive prospect of manipulating ZBP1 as a promising therapeutic target in diseases.

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Z-DNA 结合蛋白 1 协调先天免疫和炎症细胞死亡。
先天免疫不仅是宿主抵御微生物感染的第一道防线,而且对于宿主应对各种有害刺激也至关重要。Z-DNA 结合蛋白 1(ZBP1)是一种细胞膜核酸传感器,可通过其 Zα 结构域感知入侵病毒衍生的 Z 型核酸和自身核酸,从而诱导免疫细胞和非免疫细胞的炎性细胞死亡。从机理上讲,病原体或有害刺激诱导异常表达或活化的 ZBP1 可招募 TANK 结合激酶 1(TBK1)、干扰素调节因子 3(IRF3)、受体丝氨酸/苏氨酸蛋白激酶 1(RIPK1)和 RIPK3,以驱动 I 型干扰素(IFN-I)反应和激活核因子卡巴 B(NF-κB)信号。同时,ZBP1 促进 ZBP1- 和缺失黑色素瘤 2(AIM2)-PANoptosome 的组装,最终通过 caspase 3 介导的细胞凋亡、混合系激酶域类伪激酶(MLKL)介导的坏死和 gasdermin D(GSDMD)介导的热凋亡触发 PANoptosis。针对受损的线粒体 DNA,ZBP1 可与环 GMP-AMP 合成酶相互作用,增强 IFN-I 反应,但抑制收费类受体 9 介导的炎症反应。这篇综述总结了 ZBP1 的结构和表达模式,讨论了它通过免疫依赖性(如产生 IFN-I 和促炎细胞因子)和非依赖性(如激活细胞死亡)功能在人类疾病中的作用,并强调了操纵 ZBP1 作为疾病治疗靶点的诱人前景。
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来源期刊
Cytokine & Growth Factor Reviews
Cytokine & Growth Factor Reviews 生物-生化与分子生物学
CiteScore
21.10
自引率
1.50%
发文量
61
审稿时长
22 days
期刊介绍: Cytokine & Growth Factor Reviews is a leading publication that focuses on the dynamic fields of growth factor and cytokine research. Our journal offers a platform for authors to disseminate thought-provoking articles such as critical reviews, state-of-the-art reviews, letters to the editor, and meeting reviews. We aim to cover important breakthroughs in these rapidly evolving areas, providing valuable insights into the multidisciplinary significance of cytokines and growth factors. Our journal spans various domains including signal transduction, cell growth and differentiation, embryonic development, immunology, tumorigenesis, and clinical medicine. By publishing cutting-edge research and analysis, we aim to influence the way researchers and experts perceive and understand growth factors and cytokines. We encourage novel expressions of ideas and innovative approaches to organizing content, fostering a stimulating environment for knowledge exchange and scientific advancement.
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