ArticleRetrovirology2015
The role of antigen presenting cells in the induction of HIV-1 latency in resting CD4(+) T-cells.
Article in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- HIV-Associated Neurocognitive Disorder: A Look into Cellular and Molecular Pathology.International journal of molecular sciences · 2024Review
- HIV-1 Vpr Functions in Primary CD4Viruses · 2024Review
- CD8Immunity · 2023Article
- Insights into the HIV-1 Latent Reservoir and Strategies to Cure HIV-1 Infection.Disease markers · 2022Review
- Limitations of current chemotherapy and future of nanoformulation-based AmB delivery for visceral leishmaniasis-An updated review.Frontiers in bioengineering and biotechnology · 2022Review
- Article
- Flow-FISH as a Tool for Studying Bacteria, Fungi and Viruses.Biotech (Basel (Switzerland)) · 2021Review
- The multifaceted nature of HIV latency.The Journal of clinical investigation · 2020Review
- Review
- Combination Immune Checkpoint Blockade to Reverse HIV Latency.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Diverse effects of interferon alpha on the establishment and reversal of HIV latency.PLoS pathogens · 2020Article
- An elastic-net logistic regression approach to generate classifiers and gene signatures for types of immune cells and T helper cell subsets.BMC bioinformatics · 2019Article
- RGMB enhances the suppressive activity of the monomeric secreted form of CTLA-4.Scientific reports · 2019Article
- Mechanisms of HIV-1 cell-to-cell transmission and the establishment of the latent reservoir.Virus research · 2019Review
- Current Concepts on 6-sulfo LacNAc Expressing Monocytes (slanMo).Frontiers in immunology · 2019Review
- mTOR signaling mediates effects of common gamma-chain cytokines on T cell proliferation and exhaustion: implications for HIV-1 persistence and cure research.AIDS (London, England) · 2018Article
- Myeloid Dendritic Cells Induce HIV Latency in Proliferating CD4Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- CD4AIDS research and human retroviruses · 2018Review
- The Pathway To Establishing HIV Latency Is Critical to How Latency Is Maintained and Reversed.Journal of virology · 2018Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundCombination antiretroviral therapy (cART) is able to control HIV-1 viral replication, however long-lived latent infection in resting memory CD4(+) T-cells persist. The mechanisms for establishment and maintenance of latent infection in resting memory CD4(+) T-cells remain unclear. Previously we have shown that HIV-1 infection of resting CD4(+) T-cells co-cultured with CD11c(+) myeloid dendritic cells (mDC) produced a population of non-proliferating T-cells with latent infection. Here we asked whether different antigen presenting cells (APC), including subpopulations of DC and monocytes, were able to induce post-integration latent infection in resting CD4(+) T-cells, and examined potential cell interactions that may be involved using RNA-seq.
resultsmDC (CD1c(+)), SLAN(+) DC and CD14(+) monocytes were most efficient in stimulating proliferation of CD4(+) T-cells during syngeneic culture and in generating post-integration latent infection in non-proliferating CD4(+) T-cells following HIV-1 infection of APC-T cell co-cultures. In comparison, plasmacytoid DC (pDC) and B-cells did not induce latent infection in APC-T-cell co-cultures. We compared the RNA expression profiles of APC subpopulations that could and could not induce latency in non-proliferating CD4(+) T-cells. Gene expression analysis, comparing the CD1c(+) mDC, SLAN(+) DC and CD14(+) monocyte subpopulations to pDC identified 53 upregulated genes that encode proteins expressed on the plasma membrane that could signal to CD4(+) T-cells via cell-cell interactions (32 genes), immune checkpoints (IC) (5 genes), T-cell activation (9 genes), regulation of apoptosis (5 genes), antigen presentation (1 gene) and through unknown ligands (1 gene).
conclusionsAPC subpopulations from the myeloid lineage, specifically mDC subpopulations and CD14(+) monocytes, were able to efficiently induce post-integration HIV-1 latency in non-proliferating CD4(+) T-cells in vitro. Inhibition of key pathways involved in mDC-T-cell interactions and HIV-1 latency may provide novel targets to eliminate HIV-1 latency.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.