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TLR5 Signaling Stimulates the Innate Production of IL-17 and IL-22 by CD3negCD127+ Immune Cells in Spleen and Mucosa
Author(s) -
Laurye Van Maele,
Christophe Carnoy,
Delphine Cayet,
Pascal Songhet,
Laure Dumoutier,
Isabel Ferrero,
Laure Janot,
François Erard,
Julie Bertout,
Hélène Léger,
Florent Sebbane,
Arndt Benecke,
JeanChristophe Renauld,
WolfDietrich Hardt,
Bernhard Ryffel,
JeanClaude Sirard
Publication year - 2010
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1000115
Subject(s) - tlr5 , innate lymphoid cell , biology , innate immune system , immunology , flagellin , immune system , acquired immune system , interleukin 7 receptor , microbiology and biotechnology , cytotoxic t cell , t cell , toll like receptor , il 2 receptor , receptor , in vitro , genetics
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 CD3(neg)CD127(+) 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 CD3(neg)CD127(+) cells and production of Th17-related cytokines may be crucial for the early defenses against pathogen invasion of host tissues.

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