Impact of in vitro co-stimulation with of TLR2, TLR4 and TLR9 agonists and HIV1, on antigen-presenting cell activation

Objective: HIV-1 infects several immune cells including dendritic cells (DCs) and monocytes, which contributes in both to dissemination of HIV-1 infection and induction of antiviral immunity. These cells produce high amounts of type I IFN and proinflammatory cytokines upon Toll-like receptor (TLR) s...

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Autores:
Giraldo, Diana Marcela
Hernández López, Juan Carlos
Urucqui Inchima, Silvio
Tipo de recurso:
Article of journal
Fecha de publicación:
2015
Institución:
Universidad Cooperativa de Colombia
Repositorio:
Repositorio UCC
Idioma:
OAI Identifier:
oai:repository.ucc.edu.co:20.500.12494/1262
Acceso en línea:
https://hdl.handle.net/20.500.12494/1262
Palabra clave:
HIV-1
Dendritic cells
Rights
embargoedAccess
License
Licencia CC
Description
Summary:Objective: HIV-1 infects several immune cells including dendritic cells (DCs) and monocytes, which contributes in both to dissemination of HIV-1 infection and induction of antiviral immunity. These cells produce high amounts of type I IFN and proinflammatory cytokines upon Toll-like receptor (TLR) stimulation. During HIV-1 infection, an altered production of proinflammatory cytokines has been reported. However, the mechanisms underlying cytokine modulation have not been well described. Here, we evaluated the production of proinflammatory cytokines and activation of myeloid and plasmacytoid DCs and monocytes costimulated in vitro with TLR agonists and HIV-1. Methods: Changes in cytokine expression by real-time PCR and activation of DCs and monocytes by flow cytometry were evaluated after costimulation with HIV-1 and TLR agonists. Results: We observed an upregulation of TNF-α expression after TLR4 stimulation, but a downregulation of IL-6 when TLR2/TLR9 were stimulated. Interestingly, the expression of CD80 and CD86 costimulatory molecules in monocytes and DCs were significantly increased in cells challenged with HIV-1 and TLR2/TLR4/TLR9 agonists. Conclusion: This regulation of TNF-α and IL-6 production and changes in the expression of costimulatory molecules can be critical in the context of HIV-1 infection, by favoring the antigen-presenting cell activation through the stimulation of TLRs.