A new function of the Fas-FasL pathway in macrophage activation.

Détails

ID Serval
serval:BIB_154E3EF779B9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A new function of the Fas-FasL pathway in macrophage activation.
Périodique
Journal of Leukocyte Biology
Auteur(s)
Chakour R., Allenbach C., Desgranges F., Charmoy M., Mauel J., Garcia I., Launois P., Louis J., Tacchini-Cottier F.
ISSN
1938-3673[electronic]
Statut éditorial
Publié
Date de publication
2009
Peer-reviewed
Oui
Volume
86
Numéro
1
Pages
81-90
Langue
anglais
Résumé
Upon infection with the protozoan parasite Leishmania major, susceptible BALB/c mice develop unhealing lesions associated with the maturation of CD4(+)Th2 cells secreting IL-4. In contrast, resistant C57BL/6 mice heal their lesions, because of expansion and secretion of IFN-gamma of CD4(+) Th1 cells. The Fas-FasL pathway, although not involved in Th cell differentiation, was reported to be necessary for complete resolution of lesions. We investigate here the role of IFN-gamma and IL-4 on Fas-FasL nonapoptotic signaling events leading to the modulation of macrophage activation. We show that addition of FasL and IFN-gamma to BMMø led to their increased activation, as reflected by enhanced secretion of TNF, IL-6, NO, and the induction of their microbicidal activity, resulting in the killing of intracellular L. major. In contrast, the presence of IL-4 decreased the synergy of IFN-gamma/FasL significantly on macrophage activation and the killing of intracellular L. major. These results show that FasL synergizes with IFN-gamma to activate macrophages and that the tight regulation by IFN-gamma and/or IL-4 of the nonapoptotic signaling events triggered by the Fas-FasL pathway affects significantly the activation of macrophages to a microbicidal state and may thus contribute to the pathogenesis of L. major infection.
Pubmed
Web of science
Création de la notice
17/08/2009 13:06
Dernière modification de la notice
20/08/2019 13:44
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