The early IL-4 response to Leishmania major and the resulting Th2 cell maturation steering progressive disease in BALB/c mice are subject to the control of regulatory CD4+CD25+ T cells.

Détails

ID Serval
serval:BIB_CD2AD8B456FD
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
The early IL-4 response to Leishmania major and the resulting Th2 cell maturation steering progressive disease in BALB/c mice are subject to the control of regulatory CD4+CD25+ T cells.
Périodique
Journal of Immunology
Auteur(s)
Aseffa A., Gumy A., Launois P., MacDonald H.R., Louis J.A., Tacchini-Cottier F.
ISSN
0022-1767 (Print)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2002
Volume
169
Numéro
6
Pages
3232-3241
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Susceptibility and development of Th2 cells in BALB/c mice infected with Leishmania major result from early IL-4 production by Vbeta4Valpha8 CD4+ T cells in response to the Leishmania homolog of mammalian RACK1 Ag. A role for CD4+CD25+ regulatory T cells in the control of this early IL-4 production was investigated by depleting in vivo this regulatory T cell population. Depletion induced an increase in the early burst of IL-4 mRNA in the draining lymph nodes of BALB/c mice, and exacerbated the course of disease with higher levels of IL-4 mRNA and protein in their lymph nodes. We further showed that transfer of 10(7) BALB/c spleen cells that were depleted of CD4+CD25+ regulatory T cells rendered SCID mice susceptible to infection and allowed Th2 differentiation while SCID mice reconstituted with 10(7) control BALB/c spleen cells were resistant to infection with L. major and developed a Th1 response. Treatment with a mAb against IL-4 upon infection with L. major in SCID mice reconstituted with CD25-depleted spleen cells prevented the development of Th2 polarization and rendered them resistant to infection. These results demonstrate that CD4+CD25+ regulatory T cells play a role in regulating the early IL-4 mRNA and the subsequent development of a Th2 response in this model of infection.
Mots-clé
Adoptive Transfer, Animals, Antibodies, Monoclonal/administration & dosage, CD4-Positive T-Lymphocytes/immunology, CD4-Positive T-Lymphocytes/metabolism, Cell Differentiation/immunology, Disease Progression, Disease Susceptibility/immunology, Female, Interleukin-4/antagonists & inhibitors, Interleukin-4/biosynthesis, Leishmania major/immunology, Leishmaniasis, Cutaneous/immunology, Leishmaniasis, Cutaneous/pathology, Lymphocyte Activation, Lymphocyte Depletion/adverse effects, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, SCID, Receptors, Interleukin-2/biosynthesis, Spleen/cytology, Spleen/transplantation, T-Lymphocyte Subsets/immunology, T-Lymphocyte Subsets/metabolism, T-Lymphocytes, Regulatory/immunology, Th2 Cells/immunology, Th2 Cells/pathology
Pubmed
Web of science
Création de la notice
24/01/2008 15:08
Dernière modification de la notice
20/08/2019 15:47
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