The use of the murine model of infection with Leishmania major to reveal the antagonistic effects that IL-4 can exert on T helper cell development and demonstrate that these opposite effects depend upon the nature of the cells targeted for IL-4 signaling.

Détails

ID Serval
serval:BIB_221048CC105B
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
The use of the murine model of infection with Leishmania major to reveal the antagonistic effects that IL-4 can exert on T helper cell development and demonstrate that these opposite effects depend upon the nature of the cells targeted for IL-4 signaling.
Périodique
Pathologie-Biologie
Auteur(s)
Louis J.A., Gumy A., Voigt H., Launois P., Rocken M.
ISSN
0369-8114 (Print)
ISSN-L
0369-8114
Statut éditorial
Publié
Date de publication
2003
Volume
51
Numéro
2
Pages
71-73
Langue
anglais
Résumé
In contrast to mice from the majority of inbred strains, BALB mice develop aberrant Th2 responses and suffer progressive disease after infection with Leishmania major. These outcomes depend on the production of Interleukin 4, during the first 2 d of infection, by CD4+ T cells that express the Vbeta4-Valpha8 T cell receptors specific for a dominant I-A(d) restricted epitope of the LACK antigen from L. major. In contrast to this well established role of IL-4 in Th2 cell maturation, we have recently shown that, when limited to the initial period of activation of dendritic cells by L. major preceding T cell priming, IL-4 directs DCs to produce IL-12, promotes Th1 cell maturation and resistance to L. major in otherwise susceptible BALB/c mice. Thus, the antagonistic effects that IL-4 can have on Th cell development depend upon the nature of the cells (DCs or primed T cells) targeted for IL-4 signaling.
Mots-clé
Animals, Antigens, Protozoan/immunology, Cell Differentiation, Dendritic Cells/secretion, Genetic Predisposition to Disease, Histocompatibility Antigens Class II/immunology, Interferon-gamma/biosynthesis, Interferon-gamma/genetics, Interleukin-12/secretion, Interleukin-4/biosynthesis, Interleukin-4/genetics, Leishmania major/immunology, Leishmaniasis, Cutaneous/immunology, Mice, Mice, Inbred BALB C/immunology, Mice, Inbred BALB C/parasitology, Mice, Transgenic, Models, Animal, RNA, Messenger/biosynthesis, Receptors, Antigen, T-Cell, alpha-beta/immunology, Th1 Cells/cytology, Th1 Cells/immunology, Th2 Cells/cytology, Th2 Cells/immunology
Pubmed
Web of science
Création de la notice
28/01/2008 12:06
Dernière modification de la notice
20/08/2019 13:58
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