Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation.

Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation.
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DOI:
10.1038/ncomms12651
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发表时间:
2016-09-01
影响因子:
16.6
通讯作者:
Benezech, Cecile
Benezech, Cecile
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Jackson-Jones, Lucy H.;Duncan, Sheelagh M.;Magalhaes, Marlene S.;Campbell, Sharon M.;Maizels, Rick M.;McSorley, Henry J.;Allen, Judith E.;Benezech, Cecile

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脂肪相关淋巴簇(Fat-associated lymphoid clusters,FACC)是一种可诱导的结构,支持浆膜腔中快速的先天性B细胞免疫反应。关于在胸膜腔中激活BMCs的生理线索以及更普遍地控制BMCs中B细胞激活的机制知之甚少。在这里,我们表明,使用单独的模型,胸膜线虫感染Litomosoides sigmodontis和Altenaria alternata引起的急性肺部炎症,胸膜腔的炎症迅速激活纵隔和心包的心包积液。IL-33的产生是至关重要的胸膜B1细胞活化和局部IgM分泌。然而,B1细胞不是IL-33的直接靶点,而是需要IL-5来激活。此外,肺部炎症导致在肺内C中产生2型亮氨酸的先天性淋巴样细胞(ILC 2)产生IL-5增加。这些发现揭示了炎症,IL-33释放的基质细胞,ILC 2激活和胸膜B细胞激活的PBMC,导致局部和抗原特异性IgM的生产之间的联系。 浆膜腔中的脂肪相关淋巴簇(Fat-associated lymphoid clusters,CCLC)容纳快速产生IgM的B1细胞,但这些簇如何被激活以响应感染尚不清楚。在这里,作者表明,在肺部炎症或胸膜线虫感染的反应中,脂肪基质细胞衍生的IL-33激活ILC 2产生IL-5,从而驱动PBMC中的B1反应。
Fat-associated lymphoid clusters (FALC) are inducible structures that support rapid innate-like B-cell immune responses in the serous cavities. Little is known about the physiological cues that activate FALCs in the pleural cavity and more generally the mechanisms controlling B-cell activation in FALCs. Here we show, using separate models of pleural nematode infection with Litomosoides sigmodontis and Altenaria alternata induced acute lung inflammation, that inflammation of the pleural cavity rapidly activates mediastinal and pericardial FALCs. IL-33 produced by FALC stroma is crucial for pleural B1-cell activation and local IgM secretion. However, B1 cells are not the direct target of IL-33, which instead requires IL-5 for activation. Moreover, lung inflammation leads to increased IL-5 production by type 2 cytokine-producing innate lymphoid cells (ILC2) in the FALC. These findings reveal a link between inflammation, IL-33 release by FALC stromal cells, ILC2 activation and pleural B-cell activation in FALCs, resulting in local and antigen-specific IgM production. Fat-associated lymphoid clusters (FALC) in the serous cavities house rapid IgM-producing B1 cells, but how the clusters are activated to respond to infection is unclear. Here the authors show that in response to lung inflammation or pleural nematode infection adipose stromal cell-derived IL-33 activates ILC2s to produce IL-5, thus driving the B1 response in the FALCs.
DOI: 10.4049/jimmunol.1003020
发表时间: 2011-04-01
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
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