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IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation

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IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation. / Turner, Jan Eric; Morrison, Peter J; Wilhelm, Christoph; Wilson, Mark; Ahlfors, Helena; Renauld, Jean-Christophe; Panzer, Ulf; Helmby, Helena; Stockinger, Brigitta.

In: J EXP MED, Vol. 210, No. 13, 16.12.2013, p. 2951-65.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Turner, JE, Morrison, PJ, Wilhelm, C, Wilson, M, Ahlfors, H, Renauld, J-C, Panzer, U, Helmby, H & Stockinger, B 2013, 'IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation', J EXP MED, vol. 210, no. 13, pp. 2951-65. https://doi.org/10.1084/jem.20130071

APA

Turner, J. E., Morrison, P. J., Wilhelm, C., Wilson, M., Ahlfors, H., Renauld, J-C., Panzer, U., Helmby, H., & Stockinger, B. (2013). IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation. J EXP MED, 210(13), 2951-65. https://doi.org/10.1084/jem.20130071

Vancouver

Turner JE, Morrison PJ, Wilhelm C, Wilson M, Ahlfors H, Renauld J-C et al. IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation. J EXP MED. 2013 Dec 16;210(13):2951-65. https://doi.org/10.1084/jem.20130071

Bibtex

@article{5db116757b624227934d17f94a919513,
title = "IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation",
abstract = "IL-9 fate reporter mice established type 2 innate lymphoid cells (ILC2s) as major producers of this cytokine in vivo. Here we focus on the role of IL-9 and ILC2s during the lung stage of infection with Nippostrongylus brasiliensis, which results in substantial tissue damage. IL-9 receptor (IL-9R)-deficient mice displayed reduced numbers of ILC2s in the lung after infection, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2 cells. As a consequence, the restoration of tissue integrity and lung function was strongly impaired in the absence of IL-9 signaling. ILC2s, in contrast to Th2 cells, expressed high levels of the IL-9R, and IL-9 signaling was crucial for the survival of activated ILC2s in vitro. Furthermore, ILC2s in the lungs of infected mice required the IL-9R to up-regulate the antiapoptotic protein BCL-3 in vivo. This highlights a unique role for IL-9 as an autocrine amplifier of ILC2 function, promoting tissue repair in the recovery phase after helminth-induced lung inflammation.",
keywords = "Animals, Apoptosis, Cell Survival, Cytokines, Female, Flow Cytometry, Glycoproteins, Inflammation, Intercellular Signaling Peptides and Proteins, Interleukin-13, Interleukin-9, Lung, Lung Diseases, Lymphocytes, Macrophages, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Nippostrongylus, Pneumonia, Signal Transduction, Strongylida Infections",
author = "Turner, {Jan Eric} and Morrison, {Peter J} and Christoph Wilhelm and Mark Wilson and Helena Ahlfors and Jean-Christophe Renauld and Ulf Panzer and Helena Helmby and Brigitta Stockinger",
year = "2013",
month = dec,
day = "16",
doi = "10.1084/jem.20130071",
language = "English",
volume = "210",
pages = "2951--65",
journal = "J EXP MED",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "13",

}

RIS

TY - JOUR

T1 - IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation

AU - Turner, Jan Eric

AU - Morrison, Peter J

AU - Wilhelm, Christoph

AU - Wilson, Mark

AU - Ahlfors, Helena

AU - Renauld, Jean-Christophe

AU - Panzer, Ulf

AU - Helmby, Helena

AU - Stockinger, Brigitta

PY - 2013/12/16

Y1 - 2013/12/16

N2 - IL-9 fate reporter mice established type 2 innate lymphoid cells (ILC2s) as major producers of this cytokine in vivo. Here we focus on the role of IL-9 and ILC2s during the lung stage of infection with Nippostrongylus brasiliensis, which results in substantial tissue damage. IL-9 receptor (IL-9R)-deficient mice displayed reduced numbers of ILC2s in the lung after infection, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2 cells. As a consequence, the restoration of tissue integrity and lung function was strongly impaired in the absence of IL-9 signaling. ILC2s, in contrast to Th2 cells, expressed high levels of the IL-9R, and IL-9 signaling was crucial for the survival of activated ILC2s in vitro. Furthermore, ILC2s in the lungs of infected mice required the IL-9R to up-regulate the antiapoptotic protein BCL-3 in vivo. This highlights a unique role for IL-9 as an autocrine amplifier of ILC2 function, promoting tissue repair in the recovery phase after helminth-induced lung inflammation.

AB - IL-9 fate reporter mice established type 2 innate lymphoid cells (ILC2s) as major producers of this cytokine in vivo. Here we focus on the role of IL-9 and ILC2s during the lung stage of infection with Nippostrongylus brasiliensis, which results in substantial tissue damage. IL-9 receptor (IL-9R)-deficient mice displayed reduced numbers of ILC2s in the lung after infection, resulting in impaired IL-5, IL-13, and amphiregulin levels, despite undiminished numbers of Th2 cells. As a consequence, the restoration of tissue integrity and lung function was strongly impaired in the absence of IL-9 signaling. ILC2s, in contrast to Th2 cells, expressed high levels of the IL-9R, and IL-9 signaling was crucial for the survival of activated ILC2s in vitro. Furthermore, ILC2s in the lungs of infected mice required the IL-9R to up-regulate the antiapoptotic protein BCL-3 in vivo. This highlights a unique role for IL-9 as an autocrine amplifier of ILC2 function, promoting tissue repair in the recovery phase after helminth-induced lung inflammation.

KW - Animals

KW - Apoptosis

KW - Cell Survival

KW - Cytokines

KW - Female

KW - Flow Cytometry

KW - Glycoproteins

KW - Inflammation

KW - Intercellular Signaling Peptides and Proteins

KW - Interleukin-13

KW - Interleukin-9

KW - Lung

KW - Lung Diseases

KW - Lymphocytes

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Transgenic

KW - Nippostrongylus

KW - Pneumonia

KW - Signal Transduction

KW - Strongylida Infections

U2 - 10.1084/jem.20130071

DO - 10.1084/jem.20130071

M3 - SCORING: Journal article

C2 - 24249111

VL - 210

SP - 2951

EP - 2965

JO - J EXP MED

JF - J EXP MED

SN - 0022-1007

IS - 13

ER -