痘病毒的免疫逃避

IF 26.9 1区 医学 Q1 IMMUNOLOGY Annual review of immunology Pub Date : 2024-06-01 DOI:10.1146/annurev-immunol-090222-110227
Bruno Hernaez, Antonio Alcamí
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引用次数: 0

摘要

痘病毒进化出了一系列逃避免疫反应的机制,我们将概述不同的免疫调节策略。痘病毒会阻止识别引发免疫反应的病毒 DNA,并抑制感染细胞内的信号通路。痘病毒的一个独特特征是产生模拟细胞因子和细胞因子受体的分泌蛋白,作为诱饵受体中和细胞因子和趋化因子的活性。痘病毒通常通过干扰抗原递呈途径来阻断自然杀伤细胞和细胞毒性 T 细胞,这与痘病毒通过抑制细胞因子活化来逃避细胞免疫反应的策略相辅相成。痘病毒还编码了针对补体激活的机制。针对免疫分子和免疫途径的病毒编码蛋白在免疫调节中发挥着重要作用,本文讨论了它们对病毒发病机制的贡献,即促进病毒复制或预防免疫病理。
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Poxvirus Immune Evasion.

Poxviruses have evolved a wide array of mechanisms to evade the immune response, and we provide an overview of the different immunomodulatory strategies. Poxviruses prevent the recognition of viral DNA that triggers the immune responses and inhibit signaling pathways within the infected cell. A unique feature of poxviruses is the production of secreted proteins that mimic cytokines and cytokine receptors, acting as decoy receptors to neutralize the activity of cytokines and chemokines. The capacity of these proteins to evade cellular immune responses by inhibiting cytokine activation is complemented by poxviruses' strategies to block natural killer cells and cytotoxic T cells, often through interfering with antigen presentation pathways. Mechanisms that target complement activation are also encoded by poxviruses. Virus-encoded proteins that target immune molecules and pathways play a major role in immune modulation, and their contribution to viral pathogenesis, facilitating virus replication or preventing immunopathology, is discussed.

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来源期刊
Annual review of immunology
Annual review of immunology 医学-免疫学
CiteScore
57.20
自引率
0.70%
发文量
29
期刊介绍: The Annual Review of Immunology, in publication since 1983, focuses on basic immune mechanisms and molecular basis of immune diseases in humans. Topics include innate and adaptive immunity; immune cell development and differentiation; immune control of pathogens (viruses, bacteria, parasites) and cancer; and human immunodeficiency and autoimmune diseases. The current volume of this journal has been converted from gated to open access through Annual Reviews' Subscribe to Open program, with all articles published under a CC BY license.
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