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

First Author  Jackson-Jones LH Year  2016
Journal  Nat Commun Volume  7
Pages  12651 PubMed ID  27582256
Mgi Jnum  J:241900 Mgi Id  MGI:5903832
Doi  10.1038/ncomms12651 Citation  Jackson-Jones LH, et al. (2016) Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation. Nat Commun 7:12651
abstractText  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.
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