IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection.

IL-17 contributes to neutrophil recruitment but not to control of viral replication during acute mouse adenovirus type 1 respiratory infection.
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DOI:
10.1016/j.virol.2014.04.008
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发表时间:
2014-05
期刊:
影响因子:
3.7
通讯作者:
Weinberg, Jason B.
Weinberg, Jason B.
中科院分区:
医学3区
文献类型:
--
作者:
McCarthy, Mary K.;Zhu, Lingqiao;Procario, Megan C.;Weinberg, Jason B.

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产生IL-17的CD 4+辅助性T细胞(Th 17细胞)促进对许多病原体的炎症反应。我们使用小鼠腺病毒1型(MAV-1)来确定IL-17对腺病毒发病机制的贡献。MAV-1感染C57 BL/6小鼠可上调IL-17、Th 17相关因子IL-23和RORγt的表达。只有CD 4 + T细胞与病毒特异性IL-17产生相关。MAV-1感染后,IL-17−/−小鼠气道中的中性粒细胞较少,但IL-17+/+和IL-17−/−小鼠之间的肺部炎症没有其他差异。使用抗Gr-1抗体耗竭中性粒细胞的小鼠的肺病毒载量高于对照组。尽管中性粒细胞募集受损,但IL-17+/+和IL-17−/−小鼠在峰值肺病毒载量、肺病毒清除或保护性免疫建立方面没有差异。我们证明了在MAV-1呼吸道感染过程中有强大的Th 17应答,但这些应答对于控制病毒感染或病毒诱导的肺部炎症并不是必需的。
IL-17-producing CD4+ helper T cells (Th17 cells) promote inflammatory responses to many pathogens. We used mouse adenovirus type 1 (MAV-1) to determine contributions of IL-17 to adenovirus pathogenesis. MAV-1 infection of C57BL/6 mice upregulated lung expression of IL-17 and the Th17-associated factors IL-23 and RORγt. Only CD4+ T cells were associated with virus-specific IL-17 production. Fewer neutrophils were recruited to airways of IL-17−/− mice following MAV-1 infection, but there were no other differences in pulmonary inflammation between IL-17+/+ and IL-17−/− mice. Mice depleted of neutrophils using anti-Gr-1 antibody had greater lung viral loads than controls. Despite impaired neutrophil recruitment, there were no differences between IL-17+/+ and IL-17−/− mice in peak lung viral loads, clearance of virus from the lungs, or establishment of protective immunity. We demonstrate robust Th17 responses during MAV-1 respiratory infection, but these responses are not essential for control of virus infection or for virus-induced pulmonary inflammation.
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发表时间: 2009-03-15
期刊: Journal of immunology (Baltimore, Md. : 1950)
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影响因子: --
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