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| Home > Articles > Published articles > CD32 expression is associated to T-cell activation and is not a marker of the HIV-1 reservoir |
(Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa) (Institut Germans Trias i Pujol. Institut de Recerca de la Sida IrsiCaixa)| Date: | 2018 |
| Abstract: | CD32 has been shown to be preferentially expressed in latently HIV-1-infected cells in an in vitro model of quiescent CD4 T cells. Here we show that stimulation of CD4+ T cells with IL-2, IL-7, PHA, and anti-CD3/CD28 antibodies induces T-cell proliferation, co-expression of CD32 and the activation of the markers HLA-DR and CD69. HIV-1 infection increases CD32 expression. 79. 2% of the CD32+/CD4+ T cells from HIV+ individuals under antiretroviral treatment were HLA-DR+. Resting CD4+ T cells infected in vitro generally results in higher integration of provirus. We observe no difference in provirus integration or replication-competent inducible latent HIV-1 in CD32+ or CD32- CD4+ T cells from HIV+ individuals. Our results demonstrate that CD32 expression is a marker of CD4+ T cell activation in HIV+ individuals and raises questions regarding the immune resting status of CD32+ cells harboring HIV-1 proviruses. CD32 has been previously shown to be expressed preferentially by CD4 T cells latently harbouring HIV-1. Here the authors show that CD32 expression in CD4 T cells is associated with T cell activation, is up-regulated by HIV-1 infection and importantly does not appear to represent an enriched cellular niche for latent HIV-1. |
| Grants: | Ministerio de Economía y Competitividad BFU2015-63800-R Ministerio de Economía y Competitividad PI15/00492 Ministerio de Economía y Competitividad PI16/00103 Instituto de Salud Carlos III PI17/00624 |
| Rights: | Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.  |
| Language: | Anglès |
| Document: | Article ; recerca ; Versió publicada |
| Published in: | Nature communications, Vol. 9 (july 2018) , ISSN 2041-1723 |
