ArticlePloS one2008
HIV-induced type I interferon and tryptophan catabolism drive T cell dysfunction despite phenotypic activation.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- Transcriptomic meta-analysis identifies gene expression characteristics in various samples of HIV-infected patients with nonprogressive disease.Journal of translational medicine · 2017Pooled it
- A novel CD69 binding ankyrin repeat protein (AnkyronResearch square · 2026Article
- Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV.Aging · 2026Article
- HIV-1 derived oligonucleotides induce a type I IFN/STING dependent immune suppression reversible by targeting IFNARI.PLoS pathogens · 2026Article
- Metabolomics of HIV in the Modern cART Era.Advances in experimental medicine and biology · 2026Review
- Immune dysregulation in type 2 diabetes mellitus: Implications for tuberculosis, COVID-19, and HIV/AIDS.Infectious medicine · 2025Review
- HIV-1 adapts to HLA class II-associated selection pressure exerted by CD4Science advances · 2025Article
- SARS CoV-2 infection as a risk factor of preeclampsia and pre-term birth. An interplay between viral infection, pregnancy-specific immune shift and endothelial dysfunction may lead to negative pregnancy outcomes.Annals of medicine · 2023Review
- HIV-1 Infection Results in Sphingosine-1-Phosphate Receptor 1 Dysregulation in the Human Thymus.International journal of molecular sciences · 2023Article
- HIV-1-Host Interaction in Gut-Associated Lymphoid Tissue (GALT): Effects on Local Environment and Comorbidities.International journal of molecular sciences · 2023Review
- Reshaping the tumor microenvironment with oncolytic viruses, positive regulation of the immune synapse, and blockade of the immunosuppressive oncometabolic circuitry.Journal for immunotherapy of cancer · 2022Article
- Anti-type I interferon antibodies as a cause of severe COVID-19.Faculty reviews · 2022Article
- STING agonist loaded lipid nanoparticles overcome anti-PD-1 resistance in melanoma lung metastasis via NK cell activation.Journal for immunotherapy of cancer · 2021Article
- MicroRNA155 Plays a Critical Role in the Pathogenesis of Cutaneous Leishmania major Infection by Promoting a Th2 Response and Attenuating Dendritic Cell Activity.The American journal of pathology · 2021Article
- USP18 is a significant driver of memory CD4 T-cell reduced viability caused by type I IFN signaling during primary HIV-1 infection.PLoS pathogens · 2019Article
- Mental health and HIV/AIDS: the need for an integrated response.AIDS (London, England) · 2019Review
- HIV-Exposed Uninfected Infants Have Increased Regulatory T Cells That Correlate With Decreased T Cell Function.Frontiers in immunology · 2019Article
- Human Dendritic Cell Subsets, Ontogeny, and Impact on HIV Infection.Frontiers in immunology · 2019Review
- Review
- Elevated Level of CD4Frontiers in immunology · 2018Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Infection by the human immunodeficiency virus (HIV) is characterized by functional impairment and chronic activation of T lymphocytes, the causes of which are largely unexplained. We cultured peripheral blood mononuclear cells (PBMC) from HIV-uninfected donors in the presence or absence of HIV. HIV exposure increased expression of the activation markers CD69 and CD38 on CD4 and CD8 T cells. IFN-alpha/beta, produced by HIV-activated plasmacytoid dendritic cells (pDC), was necessary and sufficient for CD69 and CD38 upregulation, as the HIV-induced effect was inhibited by blockade of IFN-alpha/beta receptor and mimicked by recombinant IFN-alpha/beta. T cells from HIV-exposed PBMC showed reduced proliferation after T cell receptor stimulation, partially prevented by 1-methyl tryptophan, a competitive inhibitor of the immunesuppressive enzyme indoleamine (2,3)-dioxygenase (IDO), expressed by HIV-activated pDC. HIV-induced IDO inhibited CD4 T cell proliferation by cell cycle arrest in G1/S, and prevented CD8 T cell from entering the cell cycle by downmodulating the costimulatory receptor CD28. Finally, the expression of CHOP, a marker of the stress response activated by IDO, was upregulated by HIV in T cells in vitro and is increased in T cells from HIV-infected patients. Our data provide an in vitro model for HIV-induced T cell dysregulation and support the hypothesis that activation of pDC concomitantly contribute to phenotypic T cell activation and inhibition of T cell proliferative capacity during HIV infection.
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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.