感染引起的淋巴拉链限制了体液运输和病毒从皮肤的传播。

The Tokushima journal of experimental medicine Pub Date : 2022-05-02 Epub Date: 2022-03-30 DOI:10.1084/jem.20211830
Madeline J Churchill, Haley du Bois, Taylor A Heim, Tenny Mudianto, Maria M Steele, Jeffrey C Nolz, Amanda W Lund
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引用次数: 0

摘要

淋巴管通常被认为是将抗原物质、病原体和细胞冲向引流淋巴结的被动通道。然而,最近的证据表明,淋巴管能主动调节从抗原转运到白细胞贩运和食物脂质吸收等各种过程。在这里,我们测试了感染诱导的淋巴运输变化积极促进先天宿主防御的假设。我们证明,通过瘢痕感染皮肤疫苗病毒会激活真皮淋巴毛细血管交界处收紧(拉链)和淋巴结淋巴管生成,这与体液运输减少和皮肤病毒螯合有关。淋巴特异性删除 VEGFR2 可阻止感染诱导的淋巴毛细血管拉链,增加组织液流出,并允许病毒通过淋巴传播。此外,在缺乏淋巴 VEGFR2 的情况下,树突状细胞向淋巴结迁移的减少与抗病毒 CD8+ T 细胞扩增的减少有关。这些数据表明,VEGFR2 驱动的淋巴重塑是先天宿主防御的一种环境依赖性主动机制,它能限制病毒传播并促进保护性的抗病毒 CD8+ T 细胞反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Infection-induced lymphatic zippering restricts fluid transport and viral dissemination from skin.

Lymphatic vessels are often considered passive conduits that flush antigenic material, pathogens, and cells to draining lymph nodes. Recent evidence, however, suggests that lymphatic vessels actively regulate diverse processes from antigen transport to leukocyte trafficking and dietary lipid absorption. Here we tested the hypothesis that infection-induced changes in lymphatic transport actively contribute to innate host defense. We demonstrate that cutaneous vaccinia virus infection by scarification activates dermal lymphatic capillary junction tightening (zippering) and lymph node lymphangiogenesis, which are associated with reduced fluid transport and cutaneous viral sequestration. Lymphatic-specific deletion of VEGFR2 prevented infection-induced lymphatic capillary zippering, increased fluid flux out of tissue, and allowed lymphatic dissemination of virus. Further, a reduction in dendritic cell migration to lymph nodes in the absence of lymphatic VEGFR2 associated with reduced antiviral CD8+ T cell expansion. These data indicate that VEGFR2-driven lymphatic remodeling is a context-dependent, active mechanism of innate host defense that limits viral dissemination and facilitates protective, antiviral CD8+ T cell responses.

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