Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.12530/43209
Title: CD72/CD100 and PD-1/PD-L1 markers are increased on T and B cells in HIV-1+ viremic individuals, and CD72/CD100 axis is correlated with T-cell exhaustion.
Authors: 
Mesh: 
Issue Date: 2018
Citation: PLoS ONE.2018;(13)8:e0203419
Abstract: In our work, we analyzed the role of the CD100/CD72 and PD-1/PD-L1 axes in immune response dysfunction in human immunodeficiency virus (HIV)-1 infection in which high expressions of PD-1 and PD-L1 were associated with an immunosuppressive state via limitation of the HIV-1-specific T-cell responses. CD100 was demonstrated to play a relevant role in immune responses in various pathological processes and may be responsible for immune dysregulation during HIV-1 infection. We investigated the function of CD72/CD100, and PD-1/PDL-1 axes on T and B cells in HIV-infected individuals and in healthy individuals. We analyzed the frequencies and fluorescence intensities of these four markers on CD4+, CD8+ T and B cells. Marker expressions were increased during active HIV-1 infection. CD100 frequency on T cells was positively associated with the expression of PD-1 and PD-L1 on T cells from HIV-infected treatment-naïve individuals. In addition, the frequency of CD72-expressing T cells was associated with interferon gamma (IFN-γ) production in HIV-infected treatment-naïve individuals. Our data suggest that the CD72/CD100 and PD-1/PD-L1 axes may jointly participate in dysregulation of immunity during HIV-1 infection and could partially explain the immune systems' hyper-activation and exhaustion.
PMID: 30161254
URI: https://hdl.handle.net/20.500.12530/43209
Rights: openAccess
Appears in Collections:Fundaciones e Institutos de Investigación > IIS H. General U. Gregorio Marañón > Artículos
Fundaciones e Institutos de Investigación > IIS H. U. Ramón y Cajal > Artículos

Files in This Item:
File Description SizeFormat 
PMC6117071.pdf10.09 MBAdobe PDFThumbnail
View/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.