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Upon viral exposure myeloid and plasmacytoid dendritic cells produce 3 waves of distinct chemokines to recruit immune effectors

机译:病毒暴露后髓样细胞和浆细胞样树突状细胞产生3波不同的趋化因子以募集免疫效应子

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摘要

Host response to viral infection involves distinct effectors of innate and adaptive immunity, whose mobilization needs to be coordinated to ensure protection. Here we show that influenza virus triggers, in human blood dendritic-cell (DC) subsets (ie, plasmacytoid and myeloid DCs), a coordinated chemokine (CK) secretion program with 3 successive waves. The first one, occurring at early time points (2 to 4 hours), includes CKs potentially attracting effector cells such as neutrophils, cytotoxic T cells, and natural killer (NK) cells (CXCL16, CXCL1, CXCL2, and CXCL3). The second one occurs within 8 to 12 hours and includes CKs attracting effector memory T cells (CXCL8, CCL3, CCL4, CCL5, CXCL9, CXCL10, and CXCL11). The third wave, which occurs after 24 to 48 hours, when DCs have reached the lymphoid organs, includes CCL19, CCL22, and CXCL13, which attract naive T and B lymphocytes. Thus, human blood DC subsets carry a common program of CK production, which allows for a coordinated attraction of the different immune effectors in response to viral infection.
机译:宿主对病毒感染的反应涉及先天性和适应性免疫的不同效应子,需要协调其动员以确保得到保护。在这里,我们显示流感病毒在人血树突状细胞(DC)子集(即浆细胞样和髓样DC)中触发了连续3次协同的趋化因子(CK)分泌程序。第一个发生在早期时间点(2-4小时),包括可能吸引效应细胞的CK,例如嗜中性粒细胞,细胞毒性T细胞和自然杀伤(NK)细胞(CXCL16,CXCL1,CXCL2和CXCL3)。第二个发生在8到12小时内,包括吸引效应记忆T细胞的CK(CXCL8,CCL3,CCL4,CCL5,CXCL9,CXCL10和CXCL11)。第三波发生在24至48小时后,当DC到达淋巴器官时,包括CCL19,CCL22和CXCL13,它们吸引了天然的T和B淋巴细胞。因此,人血DC子集携带一个共同的CK产生程序,该程序可响应病毒感染而协调吸引不同的免疫效应子。

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