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首页> 外文期刊>PLoS Pathogens >CD200 Receptor Restriction of Myeloid Cell Responses Antagonizes Antiviral Immunity and Facilitates Cytomegalovirus Persistence within Mucosal Tissue
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CD200 Receptor Restriction of Myeloid Cell Responses Antagonizes Antiviral Immunity and Facilitates Cytomegalovirus Persistence within Mucosal Tissue

机译：髓样细胞反应的CD200受体限制拮抗抗病毒免疫，并促进粘膜组织内的巨细胞病毒持久性。

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CD200 receptor (CD200R) negatively regulates peripheral and mucosal innate immune responses. Viruses, including herpesviruses, have acquired functional CD200 orthologs, implying that viral exploitation of this pathway is evolutionary advantageous. However, the role that CD200R signaling plays during herpesvirus infection in vivo requires clarification. Utilizing the murine cytomegalovirus (MCMV) model, we demonstrate that CD200R facilitates virus persistence within mucosal tissue. Specifically, MCMV infection of CD200R-deficient mice (CD200R-/-) elicited heightened mucosal virus-specific CD4 T cell responses that restricted virus persistence in the salivary glands. CD200R did not directly inhibit lymphocyte effector function. Instead, CD200R-/- mice exhibited enhanced APC accumulation that in the mucosa was a consequence of elevated cellular proliferation. Although MCMV does not encode an obvious CD200 homolog, productive replication in macrophages induced expression of cellular CD200. CD200 from hematopoietic and non-hematopoietic cells contributed independently to suppression of antiviral control in vivo. These results highlight the CD200-CD200R pathway as an important regulator of antiviral immunity during cytomegalovirus infection that is exploited by MCMV to establish chronicity within mucosal tissue.
机译：CD200受体（CD200R）负调节外周和粘膜固有的免疫反应。包括疱疹病毒在内的病毒已获得功能性CD200直向同源物，这表明病毒利用该途径具有进化优势。但是，CD200R信号传导在体内疱疹病毒感染中扮演的角色需要澄清。利用鼠巨细胞病毒（MCMV）模型，我们证明CD200R促进粘膜组织内的病毒持久性。具体而言，CD200R缺陷小鼠（CD200R-/-）的MCMV感染引起粘膜病毒特异性CD4 T细胞应答增强，从而限制了唾液腺中病毒的持久性。 CD200R不直接抑制淋巴细胞效应功能。相反，CD200R-/-小鼠表现出增强的APC积累，这是由于在粘膜中细胞增殖升高的结果。尽管MCMV不编码明显的CD200同源物，但巨噬细胞中的有效复制诱导了细胞CD200的表达。来自造血和非造血细胞的CD200独立地抑制体内的抗病毒控制。这些结果突出了CD200-CD200R途径是巨细胞病毒感染期间抗病毒免疫的重要调节剂，MCMV已利用CD200-CD200R途径在粘膜组织内建立了慢性。

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