Coxsackievirus B4 Transplacental Infection ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Coxsackievirus B4 Transplacental Infection Severely Disturbs Central Tolerogenic Mechanisms in the Fetal Thymus
Auteur(s) :
Halouani, Aymen [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Michaux, Hélène [Auteur]
GIGA [Université Liège]
Jmii, Habib [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Trussart, Charlotte [Auteur]
GIGA [Université Liège]
Chahbi, Ahlem [Auteur]
University of Tunis El Manar
Martens, Henri [Auteur]
GIGA [Université Liège]
Renard, Chantal [Auteur]
GIGA-Neurosciences [Université Liège]
Aouni, Mahjoub [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Hober, Didier [Auteur]
Laboratoire de virologie - ULR 3610
Geenen, Vincent [Auteur]
GIGA [Université Liège]
Jaidane, Hela [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Michaux, Hélène [Auteur]
GIGA [Université Liège]
Jmii, Habib [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Trussart, Charlotte [Auteur]
GIGA [Université Liège]
Chahbi, Ahlem [Auteur]
University of Tunis El Manar
Martens, Henri [Auteur]
GIGA [Université Liège]
Renard, Chantal [Auteur]
GIGA-Neurosciences [Université Liège]
Aouni, Mahjoub [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Hober, Didier [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Laboratoire de virologie - ULR 3610
Geenen, Vincent [Auteur]
GIGA [Université Liège]
Jaidane, Hela [Auteur]
Laboratoire des Maladies Transmissibles et Substances Biologiquement Actives [Monastir] [LR99ES27]
Titre de la revue :
Microorganisms
Nom court de la revue :
Microorganisms
Numéro :
9
Pagination :
1537
Date de publication :
2021-07-31
ISSN :
2076-2607
Mot(s)-clé(s) en anglais :
Coxsackievirus B4
in utero infection
thymus
thymic epithelial cells
central self-tolerance
transcription factors
autoantigens
autoimmunity
in utero infection
thymus
thymic epithelial cells
central self-tolerance
transcription factors
autoantigens
autoimmunity
Discipline(s) HAL :
Sciences du Vivant [q-bio]/Médecine humaine et pathologie
Résumé en anglais : [en]
Thymus plays a fundamental role in central tolerance establishment, especially during fetal life, through the generation of self-tolerant T cells. This process consists in T cells education by presenting them tissue-restricted ...
Lire la suite >Thymus plays a fundamental role in central tolerance establishment, especially during fetal life, through the generation of self-tolerant T cells. This process consists in T cells education by presenting them tissue-restricted autoantigens promiscuously expressed by thymic epithelial cells (TECs), thus preventing autoimmunity. Thymus infection by Coxsackievirus B (CV-B) during fetal life is supposed to disturb thymic functions and, hence, to be an inducing or accelerating factor in the genesis of autoimmunity. To further investigate this hypothesis, in our current study, we analyzed thymic expression of autoantigens, at the transcriptional and protein level, following in utero infection by CV-B4. mRNA expression levels of Igf2 and Myo7, major autoantigens of pancreas and heart, respectively, were analyzed in whole thymus and in enriched TECs together along with both transcription factors, Aire and Fezf2, involved in autoantigens expression in the thymus. Results show that in utero infection by CV-B4 induces a significant decrease in Igf2 and Myo7 expression at both mRNA and protein level in whole thymus and in enriched TECs as well. Moreover, a correlation between viral load and autoantigens expression can be observed in the whole thymus, indicating a direct effect of in utero infection by CV-B4 on autoantigens expression. Together, these results indicate that an in utero infection of the thymus by CV-B4 may interfere with self-tolerance establishment in TECs by decreasing autoantigen expression at both mRNA and protein level and thereby increase the risk of autoimmunity onset.Lire moins >
Lire la suite >Thymus plays a fundamental role in central tolerance establishment, especially during fetal life, through the generation of self-tolerant T cells. This process consists in T cells education by presenting them tissue-restricted autoantigens promiscuously expressed by thymic epithelial cells (TECs), thus preventing autoimmunity. Thymus infection by Coxsackievirus B (CV-B) during fetal life is supposed to disturb thymic functions and, hence, to be an inducing or accelerating factor in the genesis of autoimmunity. To further investigate this hypothesis, in our current study, we analyzed thymic expression of autoantigens, at the transcriptional and protein level, following in utero infection by CV-B4. mRNA expression levels of Igf2 and Myo7, major autoantigens of pancreas and heart, respectively, were analyzed in whole thymus and in enriched TECs together along with both transcription factors, Aire and Fezf2, involved in autoantigens expression in the thymus. Results show that in utero infection by CV-B4 induces a significant decrease in Igf2 and Myo7 expression at both mRNA and protein level in whole thymus and in enriched TECs as well. Moreover, a correlation between viral load and autoantigens expression can be observed in the whole thymus, indicating a direct effect of in utero infection by CV-B4 on autoantigens expression. Together, these results indicate that an in utero infection of the thymus by CV-B4 may interfere with self-tolerance establishment in TECs by decreasing autoantigen expression at both mRNA and protein level and thereby increase the risk of autoimmunity onset.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
CHU Lille
CHU Lille
Collections :
Date de dépôt :
2024-01-17T22:12:56Z
2024-02-13T12:53:20Z
2024-02-13T12:53:20Z
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