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CD32 + CD4 + memory T cells are enriched for total HIV-1 DNA in tissues from humanized mice.

Authors :
Adams P
Fievez V
Schober R
Amand M
Iserentant G
Rutsaert S
Dessilly G
Vanham G
Hedin F
Cosma A
Moutschen M
Vandekerckhove L
Seguin-Devaux C
Source :
IScience [iScience] 2020 Nov 30; Vol. 24 (1), pp. 101881. Date of Electronic Publication: 2020 Nov 30 (Print Publication: 2021).
Publication Year :
2020

Abstract

CD32 has raised conflicting results as a putative marker of the HIV-1 reservoir. We measured CD32 expression in tissues from viremic and virally suppressed humanized mice treated relatively early or late after HIV-1 infection with combined antiretroviral therapy. CD32 was expressed in a small fraction of the memory CD4 <superscript>+</superscript> T-cell subsets from different tissues in viremic and aviremic mice, regardless of treatment initiation time. CD32 <superscript>+</superscript> memory CD4 <superscript>+</superscript> T cells were enriched in cell-associated (CA) HIV-1 DNA but not in CA HIV-1 RNA as compared to the CD32 <superscript>-</superscript> CD4 <superscript>+</superscript> fraction. Using multidimensional reduction analysis, several memory CD4 <superscript>+</superscript> CD32 <superscript>+</superscript> T-cell clusters were identified expressing HLA-DR, TIGIT, or PD-1. Importantly, although tissue-resident CD32 <superscript>+</superscript> CD4 <superscript>+</superscript> memory cells were enriched with translation-competent reservoirs, most of it was detected in memory CD32 <superscript>-</superscript> CD4 <superscript>+</superscript> T cells. Our findings support that CD32 labels highly activated/exhausted memory CD4 <superscript>+</superscript> T-cell subsets that contain only a small proportion of the translation-competent reservoir.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (© 2020 The Authors.)

Details

Language :
English
ISSN :
2589-0042
Volume :
24
Issue :
1
Database :
MEDLINE
Journal :
IScience
Publication Type :
Academic Journal
Accession number :
33364576
Full Text :
https://doi.org/10.1016/j.isci.2020.101881