Immune defence in mice lacking type I and/or type II interferon receptors.

Détails

ID Serval
serval:BIB_B3B9CF664377
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Immune defence in mice lacking type I and/or type II interferon receptors.
Périodique
Immunological Reviews
Auteur(s)
van den Broek M.F., Müller U., Huang S., Zinkernagel R.M., Aguet M.
ISSN
0105-2896 (Print)
ISSN-L
0105-2896
Statut éditorial
Publié
Date de publication
1995
Volume
148
Pages
5-18
Langue
anglais
Résumé
Mice lacking the receptor for type I interferon (IFN-alpha beta, A129 mice), for type II interferon (IFN-gamma, G129 mice) or for both receptors (AG129 mice) have been generated by embryonic stem cell mediated gene targeting and inter-crossing A129 x G129, respectively. The role of the two IFN systems in controlling a range of infections has been studied using these mice. Type I IFN is shown to be responsible for the immune defence against most viral infections tested (Lymphocytic Choriomeningitis Virus, Semliki Forest Virus, Theiler's Virus, Vesicular Stomatitis Virus), type II IFN seems to be of little importance. In Vaccinia Virus and Theiler's Virus infection, however, both IFN systems were found to play a nonredundant role. IFN-gamma was critical for the defence against intracellular bacteria (Mycobacterium, Listeria) and parasites (Leishmania), whereas IFN-alpha beta was not. IFN-alpha beta is produced by virus-infected cells within hours and plays an important role in preventing virus spread early. Production of IFN-gamma on the other hand needs activation of the immune system and plays a major role later, i.e. mostly during the immune response. Data obtained with the mice described here show that both IFN systems seem to have evolved to complement each other in the host defence against a wide variety of infectious agents.
Mots-clé
Animals, Antigens, CD/immunology, Antigens, CD/metabolism, Bacterial Infections/immunology, Humans, Immunity, Membrane Proteins, Mice, Parasitic Diseases/immunology, Receptor, Interferon alpha-beta, Receptors, Interferon/deficiency, Receptors, Interferon/immunology, Virus Diseases/immunology
Pubmed
Web of science
Création de la notice
28/01/2008 12:37
Dernière modification de la notice
03/03/2018 20:40
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