Mice from a genetically resistant background lacking the interferon gamma receptor are susceptible to infection with Leishmania major but mount a polarized T helper cell 1-type CD4+ T cell response.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY-NC-SA 4.0
ID Serval
serval:BIB_F4C102B72055
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Mice from a genetically resistant background lacking the interferon gamma receptor are susceptible to infection with Leishmania major but mount a polarized T helper cell 1-type CD4+ T cell response.
Périodique
Journal of Experimental Medicine
Auteur⸱e⸱s
Swihart K., Fruth U., Messmer N., Hug K., Behin R., Huang S., Del Giudice G., Aguet M., Louis J.A.
ISSN
0022-1007 (Print)
ISSN-L
0022-1007
Statut éditorial
Publié
Date de publication
1995
Volume
181
Numéro
3
Pages
961-971
Langue
anglais
Résumé
Mice with homologous disruption of the gene coding for the ligand-binding chain of the interferon (IFN) gamma receptor and derived from a strain genetically resistant to infection with Leishmania major have been used to study further the role of this cytokine in the differentiation of functional CD4+ T cell subsets in vivo and resistance to infection. Wild-type 129/Sv/Ev mice are resistant to infection with this parasite, developing only small lesions, which resolve spontaneously within 6 wk. In contrast, mice lacking the IFN-gamma receptor develop large, progressing lesions. After infection, lymph nodes (LN) and spleens from both wild-type and knockout mice showed an expansion of CD4+ cells producing IFN-gamma as revealed by measuring IFN-gamma in supernatants of specifically stimulated CD4+ T cells, by enumerating IFN-gamma-producing T cells, and by Northern blot analysis of IFN-gamma transcripts. No biologically active interleukin (IL) 4 was detected in supernatants of in vitro-stimulated LN or spleen cells from infected wild-type or deficient mice. Reverse transcription polymerase chain reaction analysis with primers specific for IL-4 showed similar IL-4 message levels in LN from both types of mice. The IL-4 message levels observed were comparable to those found in similarly infected C57BL/6 mice and significantly lower than the levels found in BALB/c mice. Anti-IFN-gamma treatment of both types of mice failed to alter the pattern of cytokines produced after infection. These data show that even in the absence of IFN-gamma receptors, T helper cell (Th) 1-type responses still develop in genetically resistant mice with no evidence for the expansion of Th2 cells.
Mots-clé
Animals, Antibodies, Monoclonal/immunology, Female, Interferon-gamma/physiology, Interleukin-12/physiology, Interleukin-4/physiology, Leishmania major, Leishmaniasis, Cutaneous/genetics, Leishmaniasis, Cutaneous/immunology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Receptors, Interferon/physiology, Th1 Cells/immunology
Pubmed
Web of science
Création de la notice
28/01/2008 11:36
Dernière modification de la notice
20/08/2019 16:21
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