Toll-like receptor and inflammasome signals converge to amplify the innate bactericidal capacity of T helper 1 cells.

Détails

ID Serval
serval:BIB_EE48781B2052
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Toll-like receptor and inflammasome signals converge to amplify the innate bactericidal capacity of T helper 1 cells.
Périodique
Immunity
Auteur(s)
O'Donnell H., Pham O.H., Li L.X., Atif S.M., Lee S.J., Ravesloot M.M., Stolfi J.L., Nuccio S.P., Broz P., Monack D.M., Baumler A.J., McSorley S.J.
ISSN
1097-4180 (Electronic)
ISSN-L
1074-7613
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
40
Numéro
2
Pages
213-224
Langue
anglais
Résumé
T cell effector functions can be elicited by noncognate stimuli, but the mechanism and contribution of this pathway to the resolution of intracellular macrophage infections have not been defined. Here, we show that CD4(+) T helper 1 (Th1) cells could be rapidly stimulated by microbe-associated molecular patterns during active infection with Salmonella or Chlamydia. Further, maximal stimulation of Th1 cells by lipopolysaccharide (LPS) did not require T-cell-intrinsic expression of toll-like receptor 4 (TLR4), interleukin-1 receptor (IL-1R), or interferon-γ receptor (IFN-γR) but instead required IL-18R, IL-33R, and adaptor protein MyD88. Innate stimulation of Th1 cells also required host expression of TLR4 and inflammasome components that together increased serum concentrations of IL-18. Finally, the elimination of noncognate Th1 cell stimulation hindered the resolution of primary Salmonella infection. Thus, the in vivo bactericidal capacity of Th1 cells is regulated by the response to noncognate stimuli elicited by multiple innate immune receptors.

Mots-clé
Animals, Bacterial Load/immunology, CD4 Antigens/immunology, Chlamydia/physiology, Flow Cytometry, Immunity, Innate/immunology, Inflammasomes/metabolism, Interleukin-18/metabolism, Mice, Mice, Inbred C57BL, Real-Time Polymerase Chain Reaction, Salmonella/physiology, Signal Transduction, Th1 Cells/immunology, Toll-Like Receptor 4/metabolism, Toll-Like Receptors/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/10/2017 11:05
Dernière modification de la notice
20/08/2019 17:15
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