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

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Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation. / Jackson-Jones, Lucy H; Duncan, Sheelagh M; Magalhaes, Marlène S; Campbell, Sharon M; Maizels, Rick M; McSorley, Henry J; Allen, Judith E; Bénézech, Cécile.

In: Nature Communications, Vol. 7, 12651, 01.09.2016.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Jackson-Jones, LH, Duncan, SM, Magalhaes, MS, Campbell, SM, Maizels, RM, McSorley, HJ, Allen, JE & Bénézech, C 2016, 'Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation', Nature Communications, vol. 7, 12651. https://doi.org/10.1038/ncomms12651

APA

Jackson-Jones, L. H., Duncan, S. M., Magalhaes, M. S., Campbell, S. M., Maizels, R. M., McSorley, H. J., Allen, J. E., & Bénézech, C. (2016). Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation. Nature Communications, 7, [12651]. https://doi.org/10.1038/ncomms12651

Vancouver

Jackson-Jones LH, Duncan SM, Magalhaes MS, Campbell SM, Maizels RM, McSorley HJ et al. Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation. Nature Communications. 2016 Sep 1;7. 12651. https://doi.org/10.1038/ncomms12651

Author

Jackson-Jones, Lucy H ; Duncan, Sheelagh M ; Magalhaes, Marlène S ; Campbell, Sharon M ; Maizels, Rick M ; McSorley, Henry J ; Allen, Judith E ; Bénézech, Cécile. / Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation. In: Nature Communications. 2016 ; Vol. 7.

Bibtex

@article{7f2a8c5a28954a62898c14620db3c9ab,
title = "Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation",
abstract = "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. ",
keywords = "Acute inflammation, B-1 cells, Infection, Lymphoid tissues",
author = "Jackson-Jones, {Lucy H} and Duncan, {Sheelagh M} and Magalhaes, {Marl{\`e}ne S} and Campbell, {Sharon M} and Maizels, {Rick M} and McSorley, {Henry J} and Allen, {Judith E} and C{\'e}cile B{\'e}n{\'e}zech",
year = "2016",
month = sep,
day = "1",
doi = "10.1038/ncomms12651",
language = "English",
volume = "7",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Fat-associated lymphoid clusters control local IgM secretion during pleural infection and lung inflammation

AU - Jackson-Jones, Lucy H

AU - Duncan, Sheelagh M

AU - Magalhaes, Marlène S

AU - Campbell, Sharon M

AU - Maizels, Rick M

AU - McSorley, Henry J

AU - Allen, Judith E

AU - Bénézech, Cécile

PY - 2016/9/1

Y1 - 2016/9/1

N2 - 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.

AB - 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.

KW - Acute inflammation

KW - B-1 cells

KW - Infection

KW - Lymphoid tissues

U2 - 10.1038/ncomms12651

DO - 10.1038/ncomms12651

M3 - Journal article

C2 - 27582256

VL - 7

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 12651

ER -