ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites
ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites
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DOI：
10.1084/jem.20180610
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发表时间：
2019-12-01
影响因子：
15.3
通讯作者：
Grencis, Richard K.
中科院分区：
文献类型：
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作者：
Campbell, Laura;Hepworth, Matthew R.;Grencis, Richard K.
宿主对寄生线虫的免疫需要产生强大的2型细胞因子应答，其特征在于产生白细胞介素13（IL-13），其驱动驱逐。在这里，我们发现肠道蠕虫感染也诱导ILC 2驱动的IL-13依赖性杯状细胞增生和远端部位（包括肺和其他粘膜屏障部位）粘蛋白（Muc 5 b和Muc 5ac）的产生增加。重要的是，我们表明，2型启动肺组织通过增加粘蛋白的生产抑制了随后的肺迁移蠕虫感染的进展，并限制其通过气道的过境。这些数据表明，由胃肠道寄生蠕虫感染诱导全身先天性粘蛋白反应，引发外周屏障部位，以防止随后的继发性蠕虫感染。这些数据表明，先天驱动的启动粘液屏障可能已经演变为保护随后的感染与多种蠕虫物种，这自然发生在流行地区。
Host immunity to parasitic nematodes requires the generation of a robust type 2 cytokine response, characterized by the production of interleukin 13 (IL-13), which drives expulsion. Here, we show that infection with helminths in the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased production of mucins (Muc5b and Muc5ac) at distal sites, including the lungs and other mucosal barrier sites. Critically, we show that type 2 priming of lung tissue through increased mucin production inhibits the progression of a subsequent lung migratory helminth infection and limits its transit through the airways. These data show that infection by gastrointestinal-dwelling helminths induces a systemic innate mucin response that primes peripheral barrier sites for protection against subsequent secondary helminth infections. These data suggest that innate-driven priming of mucus barriers may have evolved to protect from subsequent infections with multiple helminth species, which occur naturally in endemic areas.