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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Vaccinia virus decreases major histocompatibility complex (MHC) class II antigen presentation, T-cell priming, and peptide association with MHC class II.
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Vaccinia virus decreases major histocompatibility complex (MHC) class II antigen presentation, T-cell priming, and peptide association with MHC class II.

机译：牛痘病毒可降低II型主要组织相容性复合物（MHC）的抗原呈递，T细胞启动作用以及肽缔合。

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摘要

Vaccinia virus (VACV) is the current live virus vaccine used to protect humans against smallpox and monkeypox, but its use is contraindicated in several populations because of its virulence. It is therefore important to elucidate the immune evasion mechanisms of VACV. We found that VACV infection of antigen-presenting cells (APCs) significantly decreased major histocompatibility complex (MHC) II antigen presentation and decreased synthesis of 13 chemokines and cytokines, suggesting a potent viral mechanism for immune evasion. In these model systems, responding T cells were not directly affected by virus, indicating that VACV directly affects the APC. VACV significantly decreased nitric oxide production by peritoneal exudate cells and the RAW macrophage cell line in response to lipopolysaccharide (LPS) and interferon (IFN)-gamma, decreased class II MHC expression on APCs, and induced apoptosis in macrophages and dendritic cells. However, VACV decreased antigen presentation by 1153 B cells without apparent apoptosis induction, indicating that VACV differentially affects B lymphocytes and other APCs. We show that the key mechanism of VACV inhibition of antigen presentation may be its reduction of antigenic peptide loaded into the cleft of MHC class II molecules. These data indicate that VACV evades the host immune response by impairing critical functions of the APC.
机译：牛痘病毒（VACV）是当前用于保护人类免受天花和猴痘侵害的活病毒疫苗，但由于其毒性，它在某些人群中被禁忌使用。因此，重要的是阐明VACV的免疫逃逸机制。我们发现VACV感染抗原呈递细胞（APC）显着降低主要组织相容性复合物（MHC）II抗原呈递，并降低13种趋化因子和细胞因子的合成，表明有有效的病毒机制可逃避免疫。在这些模型系统中，反应性T细胞不受病毒直接影响，表明VACV直接影响APC。 VACV显着降低腹膜渗出细胞和RAW巨噬细胞系对脂多糖（LPS）和干扰素（IFN）-γ的反应产生的一氧化氮，降低APC上II类MHC的表达，并诱导巨噬细胞和树突状细胞的凋亡。但是，VACV减少了1153个B细胞的抗原呈递而没有明显的凋亡诱导，这表明VACV差异地影响B淋巴细胞和其他APC。我们表明，VACV抑制抗原呈递的关键机制可能是其减少加载到MHC II类分子裂缝中的抗原肽。这些数据表明，VACV通过削弱APC的关键功能来逃避宿主的免疫反应。

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