ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Genome-wide innate immune responses in HIV-1-infected macrophages are preserved despite attenuation of the NF-kappa B activation pathway.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Pericyte derived chemokines amplify neutrophil recruitment across the cerebrovascular endothelial barrier.Frontiers in immunology · 2022Article
- Monocytic-Myeloid Derived Suppressor Cells of HIV-Infected Individuals With Viral Suppression Exhibit Suppressed Innate Immunity toFrontiers in immunology · 2021Article
- Tuberculosis IRIS: Pathogenesis, Presentation, and Management across the Spectrum of Disease.Life (Basel, Switzerland) · 2020Review
- Transcriptome Profiling of Human Monocyte-Derived Macrophages Upon CCL2 Neutralization Reveals an Association Between Activation of Innate Immune Pathways and Restriction of HIV-1 Gene Expression.Frontiers in immunology · 2020Article
- Pathogenesis of HIV-1 and Mycobacterium tuberculosis co-infection.Nature reviews. Microbiology · 2018Review
- HIV-1 Infection Primes Macrophages Through STAT Signaling to Promote Enhanced Inflammation and Viral Replication.AIDS research and human retroviruses · 2017Article
- Cell-type-specific modulation of innate immune signalling by vitamin D in human mononuclear phagocytes.Immunology · 2017Article
- Tumor Necrosis Factor (TNF) Bioactivity at the Site of an Acute Cell-Mediated Immune Response Is Preserved in Rheumatoid Arthritis Patients Responding to Anti-TNF Therapy.Frontiers in immunology · 2017Article
- High-dose vitamin D3 reduces deficiency caused by low UVB exposure and limits HIV-1 replication in urban Southern Africans.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- HIV-1 infection of macrophages dysregulates innate immune responses to Mycobacterium tuberculosis by inhibition of interleukin-10.The Journal of infectious diseases · 2014Article
- Anti-apoptotic mechanisms of HIV: lessons and novel approaches to curing HIV.Cellular and molecular life sciences : CMLS · 2013Review
- HIV type 1 infection up-regulates TLR2 and TLR4 expression and function in vivo and in vitro.AIDS research and human retroviruses · 2012Article
- Dysregulation of macrophage-secreted cathepsin B contributes to HIV-1-linked neuronal apoptosis.PloS one · 2012Article
- The human transcriptome during nontyphoid Salmonella and HIV coinfection reveals attenuated NFkappaB-mediated inflammation and persistent cell cycle disruption.The Journal of infectious diseases · 2011Article
- Kaposi's sarcoma-associated herpesvirus vFLIP and human T cell lymphotropic virus type 1 Tax oncogenic proteins activate IkappaB kinase subunit gamma by different mechanisms independent of the physiological cytokine-induced pathways.Journal of virology · 2011Article
- Article
- Cell-to-cell transmission of retroviruses: Innate immunity and interferon-induced restriction factors.Virology · 2011Review
- Error, reproducibility and sensitivity: a pipeline for data processing of Agilent oligonucleotide expression arrays.BMC bioinformatics · 2010Article
- HIV-1 infection of macrophages is dependent on evasion of innate immune cellular activation.AIDS (London, England) · 2009Article
- Macrophage-mediated responses to Candida albicans in mice expressing the human immunodeficiency virus type 1 transgene.Infection and immunity · 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 2 institutions in 2 countries.
Funding
Abstract
Macrophages contribute to HIV-1 infection at many levels. They provide permissive cells at the site of inoculation, augment virus transfer to T cells, generate long-lived viral reservoirs, and cause bystander cell apoptosis. A body of evidence suggests that the role of macrophages in cellular host defense is also compromised by HIV-1 infection. In this respect, macrophages are potent cells of the innate immune system that initiate and regulate wide-ranging immunological responses. This study focuses on the effect of HIV-1 infection on innate immune responses by macrophages at the level of signal transduction, whole genome transcriptional profiling, and cytokine secretion. We show that in an ex vivo model, M-CSF-differentiated monocyte-derived macrophages uniformly infected with replicating CCR5-tropic HIV-1, without cytopathic effect, exhibit selective attenuation of the NF-kappaB activation pathway in response to TLR4 and TLR2 stimulation. However, functional annotation clustering analysis of genome-wide transcriptional responses to LPS stimulation suggests substantial preservation of gene expression changes at the systems level, with modest attenuation of a subset of up-regulated LPS-responsive genes, and no effect on a selection of inflammatory cytokine responses at the protein level. These results extend existing reports of inhibitory interactions between HIV-1 accessory proteins and NF-kappaB signaling pathways, and whole genome expression profiling provides comprehensive assessment of the consequent effects on immune response gene expression. Unexpectedly, our data suggest innate immune responses are broadly preserved with limited exceptions, and pave the way for further study of the complex relationship between HIV-1 and immunological pathways within macrophages.
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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.