Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity
| Auteur | NEKOUA, P MAGLOIRE | |
| Auteur | BERTIN, ANTOINE | |
| Auteur | SANE, FAMARA | |
| Auteur | ALIDJINOU, ENAGNON KAZALI | |
| Auteur | LOBERT, DELPHINE | |
| Auteur | TRAUET, JACQUES | |
| Auteur | HOBER, CHRISTINE | |
| Auteur | ENGELMANN, ILKA | |
| Auteur | MOUTAIROU, KABIROU | |
| Auteur | YESSOUFOU, AKADIRI A RACHIDI | |
| Auteur | HOBER, DIDIER | |
| Date d'ajout | 2026-06-02T16:06:57Z | |
| Date de disponibilite | 2026-06-02T16:06:57Z | |
| Date de publication | 2020 | |
| Resume | 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. | |
| DOI | 10.1007/s00018-019-03168-4 | |
| Autre identifiant | BECDB-8563 | |
| URI | https://dspace.uac.bj/handle/123456789/7684 | |
| Langue | fr | |
| Fait partie de | Cellular and Molecular Life Sciences | |
| Sujet | 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 | |
| Sujet | immunological effectors | |
| Sujet | especially natural killer (NK) cells | |
| Sujet | are supposed to clear virus-inf | |
| Titre | Pancreatic beta cells persistently infected with coxsackievirus B4 are targets of NK cell-mediated cytolytic activity | |
| Type | Article |
