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<dc:title xml:lang="fr">Une nouvelle approche de l’immunité innée lors de la toxoplasmose oculaire : le rôle méconnu des interférons de type I et III</dc:title>
<dcterms:alternative xml:lang="en">A new approach to innate immunity during ocular toxoplasmosis : the little-known role of type I and III interferons</dcterms:alternative>
<dc:subject xml:lang="fr">Toxoplasma gondii</dc:subject>
<dc:subject xml:lang="fr">Toxoplasmose oculaire</dc:subject>
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<dc:subject xml:lang="fr">Infection</dc:subject>
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<dc:subject xml:lang="fr">Rétine</dc:subject>
<dc:subject xml:lang="en">Toxoplasma gondii ; Ocular toxoplasmos</dc:subject>
<dc:subject xml:lang="en">Ocular toxoplasmosis</dc:subject>
<dc:subject xml:lang="en">Interferons</dc:subject>
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<dcterms:abstract xml:lang="fr">La toxoplasmose oculaire (TO) est une affection inflammatoire de l’œil consécutive à l’infection par le parasite protozoaire Toxoplasma gondii. L’objectif de cette étude était d’explorer le rôle de l’interféron-β (type I) et des IFNs-λ (type III) au cours de la TO. À l’aide de modèles in vitro de cultures rétiniennes humaines nous avons étudié l’expression de différentes cytokines, la prolifération parasitaire et la perméabilité de monocouches de cellules d’épithélium rétinien (RPEC) en réponse à la stimulation par des IFNs de type I et III et à l’infection. Nous montrons que la plupart des cellules testées sont réactives à la stimulation par des IFNs de type I et de type III, que l’infection par T. gondii induit l’expression d’IFNs de type I et de type III, que la stimulation de RPEC par des IFNs de type I limite la prolifération parasitaire lors de l’infection de ces cellules par T. gondii et que les IFNs-λ préviennent la disjonction des RPEC consécutive à l’infection par T. gondii.</dcterms:abstract>
<dcterms:abstract xml:lang="en">Ocular toxoplasmosis (TO) is an inflammatory condition of the eye caused by infection with the protozoan parasite Toxoplasma gondii. The aim of this study was to explore the role of interferon-β (type I) and IFNs-λ (type III) during TO. Using in vitro models of human retinal cultures, we studied the expression of different cytokines, parasitic proliferation and permeability of retinal epithelium cell monolayers (RPEC) in response to stimulation by type I &amp; III IFNs and infection. We show that most of the cells tested are reactive to stimulation by type I and type III IFNs, that infection with T. gondii induces the expression of type I and type III IFNs, that stimulation of RPEC by type I IFNs limits parasitic proliferation during the infection of these cells by T. gondii and that the IFNs-λ prevent the disjunction of the RPEC following infection by T. gondii.</dcterms:abstract>
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