ArticleJournal of immunology (Baltimore, Md. : 1950)2006
TRAIL-mediated apoptosis in HIV-1-infected macrophages is dependent on the inhibition of Akt-1 phosphorylation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Integrated bioinformatics analysis identifies hub genes and immune regulatory networks in HIV infection.Frontiers in immunology · 2025Article
- CounterAKTing HIV: Toward a "Block and Clear" Strategy?Frontiers in cellular and infection microbiology · 2022Review
- Small molecule ONC201 inhibits HIV-1 replication in macrophages via FOXO3a and TRAIL.Antiviral research · 2019Article
- Virus Infection and Death Receptor-Mediated Apoptosis.Viruses · 2017Review
- Fas Ligand-mediated cytotoxicity of CD4+ T cells during chronic retrovirus infection.Scientific reports · 2017Article
- Retrospective Proteomic Analysis of Cellular Immune Responses and Protective Correlates of p24 Vaccination in an HIV Elite Controller Using Antibody Arrays.Microarrays (Basel, Switzerland) · 2016Article
- Shift in monocyte apoptosis with increasing viral load and change in apoptosis-related ISG/Bcl2 family gene expression in chronically HIV-1-infected subjects.Journal of virology · 2015Article
- HIV-1 pathogenicity and virion production are dependent on the metabolic phenotype of activated CD4+ T cells.Retrovirology · 2014Article
- Article
- Tumor-specific CD4+ T cells develop cytotoxic activity and eliminate virus-induced tumor cells in the absence of regulatory T cells.Cancer immunology, immunotherapy : CII · 2013Article
- HIV-1 clade B and C isolates exhibit differential replication: relevance to macrophage-mediated neurotoxicity.Neurotoxicity research · 2011Article
- HIV-1 accessory protein Vpr: relevance in the pathogenesis of HIV and potential for therapeutic intervention.Retrovirology · 2011Review
- Article
- Article
- Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in central nervous system inflammation.Journal of molecular medicine (Berlin, Germany) · 2009Review
- Article
- New insights for FOXO and cell-fate decision in HIV infection and HIV associated neurocognitive disorder.Advances in experimental medicine and biology · 2009Review
- Induction of plasma (TRAIL), TNFR-2, Fas ligand, and plasma microparticles after human immunodeficiency virus type 1 (HIV-1) transmission: implications for HIV-1 vaccine design.Journal of virology · 2008Article
- Transcription factor FOXO3a mediates apoptosis in HIV-1-infected macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
HIV-1 uses mononuclear phagocytes (monocytes, tissue macrophages, and dendritic cells) as a vehicle for its own dissemination and as a reservoir for continuous viral replication. The mechanism by which the host immune system clears HIV-1-infected macrophages is not understood. TRAIL may play a role in this process. TRAIL is expressed on the cell membrane of peripheral immune cells and can be cleaved into a soluble, secreted form. The plasma level of TRAIL is increased in HIV-1-infected patients, particularly those with high viral loads. To study the effect of elevated TRAIL on mononuclear phagocytes, we used recombinant human (rh) TRAIL and human monocyte-derived macrophages (MDM) as an in vitro model. Our results demonstrated rhTRAIL-induced apoptosis in HIV-1-infected MDM and inhibited viral replication, while having a reduced effect on uninfected MDM. HIV-1 infection significantly decreased Akt-1 phosphorylation; rhTRAIL exposure further decreased Akt-1 phosphorylation. Infection with a dominant-negative Akt-1 adenovirus potentiated rhTRAIL-induced apoptosis, while constitutively active Akt-1 blocked rhTRAIL-induced apoptosis in HIV-1-infected MDM. From this data we conclude the death ligand TRAIL preferentially provokes apoptosis of HIV-1-infected MDM, and the mechanism is reliant upon the inhibition of Akt-1 phosphorylation. Understanding this mechanism may facilitate the elimination of HIV-1-infected macrophages and lead to new therapeutic avenues for treatment of HIV-1 infection.
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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.