Rapid IL-4 production by Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells in resistant mice treated once with anti-IL-12 or -IFN-gamma antibodies at the onset of infection with Leishmania major instructs Th2 cell development, resulting in nonhealing lesions.

Détails

ID Serval
serval:BIB_C2FB84A64E87
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Rapid IL-4 production by Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells in resistant mice treated once with anti-IL-12 or -IFN-gamma antibodies at the onset of infection with Leishmania major instructs Th2 cell development, resulting in nonhealing lesions.
Périodique
Journal of Immunology
Auteur(s)
Launois P., Gumy A., Himmelrich H., Locksley R.M., Röcken M., Louis J.A.
ISSN
0022-1767 (Print)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2002
Volume
168
Numéro
9
Pages
4628-4635
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: ppublish
Résumé
Rapid production of IL-4 by Leishmania homolog of mammalian RACK1 (LACK)-reactive CD4(+) T cells expressing the V beta 4-V alpha 8 TCR chains has been shown to drive aberrant Th2 cell development and susceptibility to Leishmania major in BALB/c mice. In contrast, mice from resistant strains fail to express this early IL-4 response. However, administration of either anti-IL-12 or -IFN-gamma at the initiation of infection allows the expression of this early IL-4 response in resistant mice. In this work we show that Leishmania homolog of mammalian RACK1-reactive CD4(+) T cells also expressing the V beta 4-V alpha 8 TCR chains are the source of the early IL-4 response to L. major in resistant mice given anti-IL-12 or -IFN-gamma Abs only at the onset of infection. Strikingly, these cells were found to be required for the reversal of the natural resistance of C57BL/6 mice following a single administration of anti-IL-12 or -IFN-gamma Abs. Together these results suggest that a deficiency in mechanisms capable of down-regulating the early IL-4 response to L. major contributes to the exquisite susceptibility of BALB/c mice to L. major.
Mots-clé
Animals, Antibodies/pharmacology, Antigens, Protozoan, CD4-Positive T-Lymphocytes/immunology, Cell Differentiation, Cells, Cultured, Cytokines/antagonists & inhibitors, Disease Progression, Female, Interferon-gamma/antagonists & inhibitors, Interferon-gamma/immunology, Interleukin-12/antagonists & inhibitors, Interleukin-12/immunology, Interleukin-4/biosynthesis, Interleukin-4/genetics, Kinetics, Leishmania major, Leishmaniasis, Cutaneous/immunology, Leishmaniasis, Cutaneous/pathology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Protozoan Proteins/pharmacology, RNA, Messenger/biosynthesis, Receptors, Antigen, T-Cell, alpha-beta/analysis, Receptors, Antigen, T-Cell, alpha-beta/genetics, Th2 Cells/immunology
Pubmed
Web of science
Création de la notice
28/01/2008 12:06
Dernière modification de la notice
03/03/2018 21:10
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