A role for lymphotoxin beta receptor in host defense against Mycobacterium bovis BCG infection.

Détails

ID Serval
serval:BIB_9C6B4069A24A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A role for lymphotoxin beta receptor in host defense against Mycobacterium bovis BCG infection.
Périodique
European Journal of Immunology
Auteur(s)
Lucas R., Tacchini-Cottier F., Guler R., Vesin D., Jemelin S., Olleros M.L., Marchal G., Browning J.L., Vassalli P., Garcia I.
ISSN
0014-2980 (Print)
ISSN-L
0014-2980
Statut éditorial
Publié
Date de publication
1999
Volume
29
Numéro
12
Pages
4002-4010
Langue
anglais
Résumé
To investigate the role of membrane lymphotoxin (LT)alpha1 / beta2 and its LTbeta receptor (LTbetaR) in the protective immune response to Mycobacterium bovis bacillus Calmette-Guérin (BCG) infection, we have used a soluble fusion molecule (LTbetaR-IgG1). LTbetaR-Ig treatment interferes with granuloma formation mainly in the spleen by inhibiting macrophage activation and nitric oxide synthase activity. In addition, a large accumulation of eosinophils was observed in the spleen of LTbetaR-Ig-treated infected mice. Decreased blood levels of IFN-gamma and increased IL-4 were also observed, suggesting that the LTbetaR pathway is important in BCG infection to favor a Th1 type of immune response. The treatment of transgenic mice expressing high blood levels of a soluble TNFR1-IgG3 fusion protein with LTbetaR-Ig resulted in a still higher sensitivity to BCG infection, and extensive necrosis in the spleen. In conclusion, these results suggest that the LTbetaR and the TNFR pathways are not redundant in the course of BCG infection and protective granuloma formation: the LTbetaR pathway appears to be important in spleen granuloma formation, whereas the TNFR pathway has a predominant role in other tissues.
Mots-clé
Animals, Gene Expression Regulation/immunology, Immunity/genetics, Lymphotoxin beta Receptor, Lymphotoxin-alpha/immunology, Lymphotoxin-beta, Membrane Proteins/immunology, Mice, Mice, Inbred BALB C, Mice, Transgenic, Mycobacterium bovis/immunology, Receptors, Tumor Necrosis Factor/genetics, Receptors, Tumor Necrosis Factor/immunology, Recombinant Fusion Proteins/genetics, Recombinant Fusion Proteins/immunology, Transfection, Tuberculosis/immunology
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 16:08
Dernière modification de la notice
20/08/2019 16:03
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