Details

Autor(en) / Beteiligte

• Van Maele, Laurye
• Carnoy, Christophe
• Cayet, Delphine
• Ivanov, Stoyan
• Porte, Rémi
• Deruy, Emeric
• Chabalgoity, José A.
• Renauld, Jean-Christophe
• Eberl, Gérard
• Benecke, Arndt G.
• Trottein, François
• Faveeuw, Christelle
• Sirard, Jean-Claude

Titel

Activation of Type 3 Innate Lymphoid Cells and Interleukin 22 Secretion in the Lungs During Streptococcus pneumoniae Infection

Ist Teil von

• The Journal of infectious diseases, 2014-08, Vol.210 (3), p.493-503

Ort / Verlag

Oxford: Oxford University Press

Erscheinungsjahr

2014

Link zum Volltext

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• 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.