In BALB/c mice, IL-4 production during the initial phase of infection with Leishmania major is necessary and sufficient to instruct Th2 cell development resulting in progressive disease.

Détails

ID Serval
serval:BIB_BD95C394475C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
In BALB/c mice, IL-4 production during the initial phase of infection with Leishmania major is necessary and sufficient to instruct Th2 cell development resulting in progressive disease.
Périodique
Journal of Immunology
Auteur(s)
Himmelrich H., Launois P., Maillard I., Biedermann T., Tacchini-Cottier F., Locksley R.M., Röcken M., Louis J.A.
ISSN
0022-1767 (Print)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2000
Volume
164
Numéro
9
Pages
4819-4825
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Résumé
In contrast to intact BALB/c mice, BALB/c mice rendered deficient in Vbeta4+ CD4+ T cells develop a Th1 response to infection with Leishmania major and are resistant. Vbeta4-deficient BALB/c mice are unable to generate the early IL-4 transcription occurring in Vbeta4 Valpha8 CD4+ T cells of BALB/c mice within 1 day of infection. Here we demonstrate that treatment of Vbeta4-deficient BALB/c mice with IL-4 during the first 64 h after infection instructs Th2 cell development and susceptibility to infection. The demonstrated inability of IL-4 to reverse the resistant phenotype of BALB/c mice treated with anti-CD4 mAb the day before infection suggest that these effects of IL-4 require its interaction with CD4+ T cells. In contrast to draining lymph node cells from BALB/c mice, cells from Vbeta4-deficient BALB/c mice remain responsive to IL-12 following infection. Strikingly, administration of IL-4 to Vbeta4-deficient BALB/c mice renders their lymph node cells unresponsive to IL-12 by down-regulating IL-12R beta2-chain expression. This study directly demonstrates that in BALB/c mice IL-4 is necessary and sufficient to initiate the molecular events steering Th2 cell maturation and susceptibility to L. major.
Mots-clé
Animals, CD4-Positive T-Lymphocytes/metabolism, CD4-Positive T-Lymphocytes/pathology, Cell Differentiation/genetics, Cell Differentiation/immunology, Disease Progression, Down-Regulation/immunology, Female, Immune Tolerance/genetics, Immunity, Innate/genetics, Injections, Intraperitoneal, Interleukin-12/metabolism, Interleukin-12/pharmacology, Interleukin-4/administration & dosage, Interleukin-4/biosynthesis, Leishmania major/immunology, Leishmaniasis, Cutaneous/genetics, Leishmaniasis, Cutaneous/immunology, Lymph Nodes/cytology, Lymph Nodes/immunology, Lymphopenia/genetics, Lymphopenia/immunology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Receptors, Antigen, T-Cell, alpha-beta/genetics, Receptors, Interleukin/antagonists & inhibitors, Receptors, Interleukin/biosynthesis, Receptors, Interleukin-12, Th2 Cells/immunology, Th2 Cells/metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 16:08
Dernière modification de la notice
03/03/2018 20:58
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