Published in
American Association of Immunologists, The Journal of Immunology, 2(185), p. 1177-1185, 2010
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- [www.ncbi.nlm.nih.gov] | PDF
- [www.ncbi.nlm.nih.gov] | PDF
- [www.hal.inserm.fr] | PDF
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TLR5 Signaling Stimulates the Innate Production of IL-17 and IL-22 by CD3negCD127+ Immune Cells in Spleen and Mucosa
,
Christophe Carnoy,
Delphine Cayet,
Pascal Songhet,
Laure Dumoutier,
Isabel Ferrero,
Laure Janot,
François Erard,
Julie Bertout,
Hélène Leger,
Florent Sebbane,
Arndt Benecke,
Jean-Christophe Renauld ,
Wolf-Dietrich Hardt
and other authors.
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Abstract
Abstract In adaptive immunity, Th17 lymphocytes produce the IL-17 and IL-22 cytokines that stimulate mucosal antimicrobial defenses and tissue repair. In this study, we observed that the TLR5 agonist flagellin induced swift and transient transcription of genes encoding IL-17 and IL-22 in lymphoid, gut, and lung tissues. This innate response also temporarily enhanced the expression of genes associated with the antimicrobial Th17 signature. The source of the Th17-related cytokines was identified as novel populations of CD3negCD127+ immune cells among which CD4-expressing cells resembling lymphoid tissue inducer cells. We also demonstrated that dendritic cells are essential for expression of Th17-related cytokines and so for stimulation of innate cells. These data define that TLR-induced activation of CD3negCD127+ cells and production of Th17-related cytokines may be crucial for the early defenses against pathogen invasion of host tissues.