期刊
JOURNAL OF INFECTIOUS DISEASES
卷 210, 期 3, 页码 493-503出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiu106
关键词
Innate lymphoid cells; interleukin-22; Toll-like receptor 5; Streptococcus pneumoniae
资金
- INSERM, Institut Pasteur de Lille, and Univ Lille Nord de France
- Region Nord Pas de Calais [ARCir Europe R07028EE]
- European Community [SavinMucoPath INCO-CT-2006-032296]
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 ROR gamma t. 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.
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