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Assessing the Impact of Persistent HIV Infection on Innate Lymphoid Cells Using In Vitro Models.
Boulay, Aude; Trabanelli, Sara; Boireau, Stéphanie; Boyer-Clavel, Myriam; Nisole, Sébastien; Romero, Pedro; Jandus, Camilla; Beignon, Anne-Sophie; Arhel, Nathalie J.
Afiliación
  • Boulay A; Viral Trafficking, Restriction and Innate Signaling, Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier, CNRS, Montpellier, France.
  • Trabanelli S; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
  • Boireau S; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland.
  • Boyer-Clavel M; Montpellier Ressources Imagerie, Biocampus, Université de Montpellier, CNRS, Montpellier, France.
  • Nisole S; Montpellier Ressources Imagerie, Biocampus, Université de Montpellier, CNRS, Montpellier, France.
  • Romero P; Viral Trafficking, Restriction and Innate Signaling, Institut de Recherche en Infectiologie de Montpellier (IRIM), Université de Montpellier, CNRS, Montpellier, France.
  • Jandus C; Department of Oncology, University of Lausanne, Épalinges, Switzerland.
  • Beignon AS; Department of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
  • Arhel NJ; Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland.
Immunohorizons ; 7(3): 243-255, 2023 03 01.
Article en En | MEDLINE | ID: mdl-37000496
Pathogens that persist in their host induce immune dysfunctions even in the absence of detectable replication. To better understand the phenotypic and functional changes that persistent infections induce in sentinel innate immune cells, we developed human PBMC-based HIV models of persistent infection. Autologous nonactivated PBMCs were cocultured with chronically infected, acutely infected, or uninfected cells and were then analyzed by unsupervised high-dimensional flow cytometry. Using this approach, we identified prevalent patterns of innate immune dysfunctions associated with persistent HIV infections that at least in part mirror immune dysfunctions observed in patients. In one or more models of chronic infection, bystander CD16+ NK cells expressing markers of activation, such as CD94, CD45RO, CD62L, CD69, CD25, and immune checkpoints PD1, Tim3, TIGIT, NKG2A and Lag3, were significantly reduced. Conversely, helper ILC subsets expressing PDL1/PDL2 were significantly enriched in chronic infection compared with either uninfected or acute infection, suggesting that chronic HIV-1 infection was associated with an inhibitory environment for bystander ILC and NK subsets. The cell-based models of persistent infection that we describe here provide versatile tools to explore the molecular mechanisms of these immune dysfunctions and unveil the contribution of innate immunity in sustaining pathogen persistence.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por VIH Límite: Humans Idioma: En Revista: Immunohorizons Año: 2023 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por VIH Límite: Humans Idioma: En Revista: Immunohorizons Año: 2023 Tipo del documento: Article País de afiliación: Francia Pais de publicación: Estados Unidos