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J Infect Dis. 2014 Aug 1;210(3):493-503. doi: 10.1093/infdis/jiu106. Epub 2014 Feb 26.

Activation of Type 3 innate lymphoid cells and interleukin 22 secretion in the lungs during Streptococcus pneumoniae infection.

Author information

1
Centre d'Infection et d'Immunité de Lille, Institut Pasteur de Lille Institut National de la Santé et de la Recherche Médicale, U1019 Centre National de la Recherche Scientifique, UMR 8204 Univ Lille Nord de France, Lille.
2
Laboratory for Vaccine Research, Department of Biotechnology, Instituto de Higiene, Facultad de Medicina, Universidad de la Republica, Montevideo, Uruguay.
3
Ludwig Institute for Cancer Research, Brussels Branch de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
4
Lymphoid Tissue Development Unit, Institut Pasteur Centre National de la Recherche Scientifique, URA 1961, Paris.
5
Institut des Hautes Études Scientifiques Centre National de la Recherche Scientifique, Bures-sur-Yvette, France.

Abstract

Mucosal sites are continuously exposed to pathogenic microorganisms and are therefore equipped to control respiratory infections. Type 3 innate lymphoid cells (ILC3) are key players in antimicrobial defense in intestinal mucosa, through interleukin 17 and interleukin 22 (IL-22) production. The present study aimed at analyzing the distribution and function of ILC3 in the respiratory tract. We first observed that lung mucosa harbors a discrete population of ILC3 expressing CD127, CD90, CCR6, and the transcriptional factor RORγt. In addition, lung ILC3 were identified as a major source of IL-22 in response to interleukin 23 stimulation. During Streptococcus pneumoniae infection, ILC3 rapidly accumulated in the lung tissue to produce IL-22. In response to S. pneumoniae, dendritic cells and MyD88, an important adaptor of innate immunity, play critical functions in IL-22 production by ILC3. Finally, administration of the Toll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by ILC3, a process that protects against lethal infection. In conclusion, boosting lung ILC3 might represent an interesting strategy to fight respiratory bacterial infections.

KEYWORDS:

Innate lymphoid cells; Streptococcus pneumoniae; Toll-like receptor 5; interleukin-22

PMID:
24577508
DOI:
10.1093/infdis/jiu106
[Indexed for MEDLINE]

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