Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins.
Th17 cytokines are critical for respiratory syncytial virus-associated airway hyperreponsiveness through regulation by complement C3a and tachykinins.
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DOI：
10.4049/jimmunol.1101789
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发表时间：
2011-10-15
期刊：
影响因子：
--
通讯作者：
Gerard NP
中科院分区：
文献类型：
--
作者：
Bera MM;Lu B;Martin TR;Cui S;Rhein LM;Gerard C;Gerard NP
Respiratory syncytial virus (RSV) infection is associated with serious lung disease in infants and immunocompromised individuals and is linked to development of asthma. In mice, acute RSV infection causes airway hyperresponsiveness (AHR), inflammation, and mucus hypersecretion. Infected cells induce complement activation, producing the anaphylatoxin C3a. Here we show RSV infected wild type mice produce Th17 cytokines, a response not previously associated with viral infections. Mice deficient in the C3aR (C3aR1−/−) fail to develop AHR following acute RSV infection, and production of Th17 cytokines was significantly attenuated. Tachykinin production has also been implicated in RSV pathophysiology, and tachykinin receptor null mice (TACR1−/−) were similarly protected from developing AHR. These animals were also deficient in production of Th17 cytokines. Tachykinin release was absent in C3aR1−/− mice, while C3a levels were unchanged in TACR1−/− animals. Thus, our data reveal a crucial sequence following acute RSV infection where initial C3a production causes tachykinin release, followed by activation of the IL-17A pathway. Deficiency of either receptor affords protection from AHR, identifying two potential therapeutic targets.
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影响因子：
64.5
作者：
Ivanov, Ivaylo I.;McKenzie, Brent S.;Littman, Dan R.
通讯作者：
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影响因子：
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DOI：
10.1016/j.jcv.2004.03.018
发表时间：
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期刊：
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