Pancreatic beta cells persistently infected ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity.
Auteur(s) :
Nekoua, Magloire Pandoua [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Bertin, Antoine [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Sane, Famara [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Alidjinou, Enagnon Kazali [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Lobert, Delphine [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Trauet, Jacques [Auteur]
Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286
Hober, Christine [Auteur]
Engelmann, Ilka [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Moutairou, Kabirou [Auteur]
Institut des Sciences Biomédicales Appliquées [ISBA]
Yessoufou, Akadiri [Auteur]
Institut des Sciences Biomédicales Appliquées [ISBA]
Hober, Didier [Auteur]
Laboratoire de virologie - ULR 3610
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Bertin, Antoine [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Sane, Famara [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Alidjinou, Enagnon Kazali [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Lobert, Delphine [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Trauet, Jacques [Auteur]
Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286
Hober, Christine [Auteur]
Engelmann, Ilka [Auteur]
Laboratoire de Virologie - ULR 3610 [Laboratoire de Virologie]
Moutairou, Kabirou [Auteur]
Institut des Sciences Biomédicales Appliquées [ISBA]
Yessoufou, Akadiri [Auteur]
Institut des Sciences Biomédicales Appliquées [ISBA]
Hober, Didier [Auteur]
Laboratoire de virologie - ULR 3610
Titre de la revue :
Cellular and Molecular Life Sciences
Nom court de la revue :
Cell. Mol. Life Sci.
Numéro :
77
Pagination :
179–194
Date de publication :
2019-06-08
ISSN :
1420-9071
Mot(s)-clé(s) en anglais :
Enterovirus
Persistence
HLA class I
Type 1 diabetes
LDH assay
Persistence
HLA class I
Type 1 diabetes
LDH assay
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
It has been suggested that the persistence of coxsackieviruses-B (CV-B) in pancreatic beta cells plays a role in the pathogenesis of type 1 diabetes (T1D). Yet, immunological effectors, especially natural killer (NK) cells, ...
Lire la suite >It has been suggested that the persistence of coxsackieviruses-B (CV-B) in pancreatic beta cells plays a role in the pathogenesis of type 1 diabetes (T1D). Yet, immunological effectors, especially natural killer (NK) cells, are supposed to clear virus-infected cells. Therefore, an evaluation of the response of NK cells to pancreatic beta cells persistently infected with CV-B4 was conducted. A persistent CV-B4 infection was established in 1.1B4 pancreatic beta cells. Infectious particles were found in supernatants throughout the culture period. The proportion of cells containing viral protein VP1 was low (< 5%), although a large proportion of cells harbored viral RNA (around 50%), whilst cell viability was preserved. HLA class I cell surface expression was downregulated in persistently infected cultures, but HLA class I mRNA levels were unchanged in comparison with mock-infected cells. The cytolytic activities of IL-2-activated non-adherent peripheral blood mononuclear cells (PBMCs) and of NK cells were higher towards persistently infected cells than towards mock-infected cells, as assessed by an LDH release assay. Impaired cytolytic activity of IL-2-activated non-adherent PBMCs from patients with T1D towards infected beta cells was observed. In conclusion, pancreatic beta cells persistently infected with CV-B4 can be lysed by NK cells, implying that impaired cytolytic activity of these effector cells may play a role in the persistence of CV-B in the host and thus in the viral pathogenesis of T1D.Lire moins >
Lire la suite >It has been suggested that the persistence of coxsackieviruses-B (CV-B) in pancreatic beta cells plays a role in the pathogenesis of type 1 diabetes (T1D). Yet, immunological effectors, especially natural killer (NK) cells, are supposed to clear virus-infected cells. Therefore, an evaluation of the response of NK cells to pancreatic beta cells persistently infected with CV-B4 was conducted. A persistent CV-B4 infection was established in 1.1B4 pancreatic beta cells. Infectious particles were found in supernatants throughout the culture period. The proportion of cells containing viral protein VP1 was low (< 5%), although a large proportion of cells harbored viral RNA (around 50%), whilst cell viability was preserved. HLA class I cell surface expression was downregulated in persistently infected cultures, but HLA class I mRNA levels were unchanged in comparison with mock-infected cells. The cytolytic activities of IL-2-activated non-adherent peripheral blood mononuclear cells (PBMCs) and of NK cells were higher towards persistently infected cells than towards mock-infected cells, as assessed by an LDH release assay. Impaired cytolytic activity of IL-2-activated non-adherent PBMCs from patients with T1D towards infected beta cells was observed. In conclusion, pancreatic beta cells persistently infected with CV-B4 can be lysed by NK cells, implying that impaired cytolytic activity of these effector cells may play a role in the persistence of CV-B in the host and thus in the viral pathogenesis of T1D.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
CHU Lille
CHU Lille
Collections :
Date de dépôt :
2024-01-17T22:32:05Z
2024-02-08T08:54:22Z
2024-02-08T08:54:22Z