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

作者：Van Maele Laurye; Carnoy Christophe; Cayet Delphine; Ivanov Stoyan; Porte Remi; Deruy Emeric; Chabalgoity Jose A; Renauld Jean Christophe; Eberl Gerard; Benecke Arndt G; Trottein Francois; Faveeuw Christelle; Sirard Jean Claude^*

来源：Journal of Infectious Diseases, 2014, 210(3): 493-503.

DOI：10.1093/infdis/jiu106

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

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.

• 出版日期2014-8-1