Platelet-derived major histocompatibility complex class I coating on Treponema pallidum attenuates natural killer cell lethality.

IF 5.5 1区 农林科学 Q1 IMMUNOLOGY Virulence Pub Date : 2024-12-01 Epub Date: 2024-05-14 DOI:10.1080/21505594.2024.2350892
Qiu-Yan Xu, Xin-Qi Zheng, Wei-Ming Ye, Dong-Yu Yi, Ze Li, Qing-Qi Meng, Man-Li Tong, Dan Liu, Tian-Ci Yang
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Abstract

The evasive tactics of Treponema pallidum pose a major challenge in combating and eradicating syphilis. Natural killer (NK) cells mediate important effector functions in the control of pathogenic infection, preferentially eliminating targets with low or no expression of major histocompatibility complex (MHC) class I. To clarify T. pallidum's mechanisms in evading NK-mediated immunosurveillance, experiments were performed to explore the cross-talk relations among T. pallidum, NK cells, and platelets. T. pallidum adhered to, activated, and promoted particle secretion of platelets. After preincubation with T. pallidum, platelets expressed and secreted high levels of MHC class I, subsequently transferring them to the surface of T. pallidum, potentially inducing an immune phenotype characterized by the "pseudo-expression" of MHC class I on the surface of T. pallidum (hereafter referred to a "pseudo-expression" of MHC class I). The polA mRNA assay showed that platelet-preincubated T. pallidum group exhibited a significantly higher copy number of polA transcript than the T. pallidum group. The survival rate of T. pallidum mirrored that of polA mRNA, indicating that preincubation of T. pallidum with platelets attenuated NK cell lethality. Platelets pseudo-expressed the MHC class I ligand on the T. pallidum surface, facilitating binding to killer cell immunoglobulin-like receptors with two immunoglobulin domains and long cytoplasmic tail 3 (KIR2DL3) on NK cells and initiating dephosphorylation of Vav1 and phosphorylation of Crk, ultimately attenuating NK cell lethality. Our findings elucidate the mechanism by which platelets transfer MHC class I to the T. pallidum surface to evade NK cell immune clearance.

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苍白螺旋体上的血小板源性主要组织相容性复合体 I 类涂层可减轻自然杀伤细胞的致死率。
苍白盘尾丝菌的躲避策略给抗击和根除梅毒带来了重大挑战。为了弄清苍白螺旋体逃避NK介导的免疫监视的机制,研究人员进行了实验来探索苍白螺旋体、NK细胞和血小板之间的交叉对话关系。苍白球粘附、激活并促进血小板分泌微粒。与苍白球预孵育后,血小板表达并分泌高水平的 MHC I 类,随后将其转移到苍白球表面,可能诱导出一种以苍白球表面 MHC I 类 "伪表达"(以下简称 MHC I 类 "伪表达")为特征的免疫表型。polA mRNA 检测显示,血小板预培养 T. pallidum 组的 polA 转录本拷贝数明显高于 T. pallidum 组。T. pallidum的存活率与polA mRNA的存活率一致,这表明T. pallidum与血小板预孵育可减轻NK细胞的致死率。血小板在苍白球表面伪表达了MHC I类配体,促进了与NK细胞上具有两个免疫球蛋白结构域和长胞质尾3(KIR2DL3)的杀伤细胞免疫球蛋白样受体的结合,并启动了Vav1的去磷酸化和Crk的磷酸化,最终降低了NK细胞的致死率。我们的发现阐明了血小板将 MHC I 类转移到苍白球表面以逃避 NK 细胞免疫清除的机制。
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来源期刊
Virulence
Virulence IMMUNOLOGY-MICROBIOLOGY
CiteScore
9.20
自引率
1.90%
发文量
123
审稿时长
6-12 weeks
期刊介绍: Virulence is a fully open access peer-reviewed journal. All articles will (if accepted) be available for anyone to read anywhere, at any time immediately on publication. Virulence is the first international peer-reviewed journal of its kind to focus exclusively on microbial pathogenicity, the infection process and host-pathogen interactions. To address the new infectious challenges, emerging infectious agents and antimicrobial resistance, there is a clear need for interdisciplinary research.
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