ArticleJournal of virology2003
Monocytes treated with human immunodeficiency virus Tat kill uninfected CD4(+) cells by a tumor necrosis factor-related apoptosis-induced ligand-mediated mechanism.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 92 citations in OpenAlex.
- TRAIL (DR5) receptor and the modulation of TRAIL pathway in PLWHIV: key mechanisms in the progression of HIV disease.BMC molecular and cell biology · 2025Article
- TRAIL promotes the polarization of human macrophages toward a proinflammatory M1 phenotype and is associated with increased survival in cancer patients with high tumor macrophage content.Frontiers in immunology · 2023Article
- HIV, Combination Antiretroviral Therapy, and Vascular Diseases in Men and Women.JACC. Basic to translational science · 2022Review
- SMAC Mimetics as Therapeutic Agents in HIV Infection.Frontiers in immunology · 2021Review
- Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020Review
- HIV elite control is associated with reduced TRAILshort expression.AIDS (London, England) · 2019Observational
- Virus Infection and Death Receptor-Mediated Apoptosis.Viruses · 2017Review
- Review
- Alterations in P-Glycoprotein Expression and Function Between Macrophage Subsets.Pharmaceutical research · 2016Article
- Colony-Stimulating Factor 1 Receptor Antagonists Sensitize Human Immunodeficiency Virus Type 1-Infected Macrophages to TRAIL-Mediated Killing.Journal of virology · 2016Article
- Review
- Review
- The macrophage: a therapeutic target in HIV-1 infection.Molecular and cellular therapies · 2014Review
- HIV and Bone Disease: A Perspective of the Role of microRNAs in Bone Biology upon HIV Infection.Journal of osteoporosis · 2013Review
- Isolation of a TRAIL antagonist from the serum of HIV-infected patients.The Journal of biological chemistry · 2011Article
- The death-promoting molecule tumour necrosis factor-related apoptosis inducing ligand (TRAIL) is not required for the development of peripheral lymphopenia or granuloma necrosis during infection with virulent Mycobacterium avium.Clinical and experimental immunology · 2011Article
- Human immunodeficiency virus viral protein R as an extracellular protein in neuropathogenesis.Advances in virus research · 2011Review
- Mechanisms of HIV-associated lymphocyte apoptosis: 2010.Cell death & disease · 2010Review
- Role of the Fas/FasL pathway in HIV or SIV disease.Retrovirology · 2009Review
- Anti-apoptotic genes in the survival of monocytic cells during infection.Current genomics · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The human immunodeficiency virus (HIV) Tat protein has a critical role in viral transcription, but this study focuses on its additional role as an extracellular effector of lymphocyte cell death. It is well known that Tat induces tumor necrosis factor-related apoptosis-induced ligand (TRAIL) in peripheral blood mononuclear cells (PBMC), and we show that the majority of TRAIL is produced by the monocyte subset of PBMC. Human monocytes and U937 monoblastoid cells did not take up soluble HIV Tat-86, as T cells did, yet produced more TRAIL than did T cells. TRAIL secretion was induced by Tat and by a cysteine-rich peptide of Tat but not by sulfhydryl-modified Tat toxoid. Although there was only a slight increase in cell surface expression of TRAIL on monocytes, sufficient TRAIL was secreted to be toxic for T cells. The cytotoxicity of Tat-stimulated monocyte medium could be blocked by a TRAIL-neutralizing antibody. T cells treated with Tat did not secrete enough TRAIL to mediate cell death in our assay. Remarkably, uninfected T cells are more susceptible to TRAIL than are HIV-infected T cells. The production of TRAIL by Tat-stimulated monocytes provides a mechanism by which HIV infection can destroy uninfected bystander cells.
Indexed as
Identifiers
What OpenQuestion holds
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.