Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection
Complement component C3 promotes T-cell priming and lung migration to control acute influenza virus infection
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DOI：
10.1038/nm0402-373
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发表时间：
2002-04-01
期刊：
影响因子：
82.9
通讯作者：
Bachmann, MF
中科院分区：
文献类型：
--
作者：
Kopf, M;Abel, B;Bachmann, MF
补体级联定义了先天免疫系统和特异性免疫系统之间的重要联系。在这里，我们表明，小鼠缺乏的第三种成分的补体（C3（-/-）小鼠）是非常容易感染流感病毒的主要。C3（-/-）小鼠表现出延迟的病毒清除和增加的病毒滴度在肺中，而补体受体CR 1和CR2缺陷的小鼠（Cr2（-/-）小鼠）清除感染正常。在C3（-/-）小鼠中，肺引流淋巴结中辅助性T细胞和细胞毒性T细胞（CTL）的引发减少，产生干扰素-γ的病毒特异性CD 4（+）和CD 8（+）效应T细胞向肺中的募集严重受损，但在Cr2（-/-）小鼠中没有。因此，C3（-/-）小鼠中T辅助细胞依赖性IgG应答降低，但Cr2（-/-）小鼠中保持完整。这些结果表明，补体通过促进T细胞应答诱导特异性免疫。
The complement cascade defines an important link between the innate and the specific immune system. Here we show that mice deficient for the third component of complement (C3(-/-) mice) are highly susceptible to primary infection with influenza virus. C3(-/-) mice showed delayed viral clearance and increased viral titers in lung, whereas mice deficient for complement receptors CR1 and CR2 (Cr2(-/-) mice) cleared the infection normally. Priming of T-helper cells and cytotoxic T cells ( CTLs) in lung-draining lymph nodes was reduced, and the recruitment into the lung of virus-specific CD4(+) and CD8(+) effector T cells producing interferon-gamma was severely impaired in C3(-/-) but not in Cr2(-/-) mice. Consequently, T-helper cell dependent IgG responses were reduced in C3(-/-) mice but remained intact in Cr2(-/-) mice. These results demonstrate that complement induces specific immunity by promoting T-cell responses.