ArticleCurrent HIV research2014
HIV-1 Tat disrupts CX3CL1-CX3CR1 axis in microglia via the NF-κBYY1 pathway.
Article in Current HIV research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Implications and prospects of immunological and neuroimaging research in HIV-associated neurocognitive disorders.Frontiers in neurologyPooled it
- Implications of HIV persistence and pathogenesis in microglia.Current opinion in HIV and AIDS · 2026Review
- The prefrontal cortex as a target of HIV-1 neurotoxicity: molecular mechanisms of viral protein-mediated neurodegeneration and executive dysfunction.Frontiers in cellular neuroscience · 2026Review
- AAV-mediated STC-1 expression mitigates neuroinflammation and preserves visual function in degenerative retinopathy.Journal of translational medicine · 2025Article
- EcoHIV infection effects on cocaine seeking and neuroimmune responses in male mice depend on cocaine exposure pattern.Addiction neuroscience · 2025Article
- Prenatal Immune Challenge Differentiates the Effect of Aripiprazole and Risperidone on CD200-CD200R and CX3CL1-CX3CR1 Dyads and Microglial Polarization: A Study in Organotypic Cortical Cultures.Life (Basel, Switzerland) · 2024Article
- Alterations in CX3CL1 Levels and Its Role in Viral Pathogenesis.International journal of molecular sciences · 2024Review
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- Blood monocyte and dendritic cell profiles among people living with HIV with Mycobacterium tuberculosis co-infection.BMC immunology · 2023Article
- Miltefosine as a PPM1A activator improves AD-like pathology in mice by alleviating tauopathy via microglia/neurons crosstalk.Brain, behavior, & immunity - health · 2022Article
- Neuroinflammatory Profiling in SIV-Infected Chinese-Origin Rhesus Macaques on Antiretroviral Therapy.Viruses · 2022Article
- The Function of NF-Kappa B During Epilepsy, a Potential Therapeutic Target.Frontiers in neuroscience · 2022Review
- Reduced neuronal population in the dorsolateral prefrontal cortex in infant macaques infected with simian immunodeficiency virus (SIV).Journal of neurovirology · 2021Article
- Neurodevelopmental Processes in the Prefrontal Cortex Derailed by Chronic HIV-1 Viral Protein Exposure.Cells · 2021Article
- HIV-Associated Apathy/Depression and Neurocognitive Impairments Reflect Persistent Dopamine Deficits.Cells · 2021Review
- HIV-1 TAT-mediated microglial activation: role of mitochondrial dysfunction and defective mitophagy.Autophagy · 2018Article
- Emerging roles of extracellular vesicles in neurodegenerative disorders: focus on HIV-associated neurological complications.Cell death & disease · 2016Review
- Mesenchymal Stem Cells Modulate the Functional Properties of Microglia via TGF-β Secretion.Stem cells translational medicine · 2016Article
- Crocin Upregulates CX3CR1 Expression by Suppressing NF-κB/YY1 Signaling and Inhibiting Lipopolysaccharide-Induced Microglial Activation.Neurochemical research · 2016Article
- Immune activation in the central nervous system throughout the course of HIV infection.Current opinion in HIV and AIDS · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Microglia are critical for the pathogenesis of HIV-associated dementia not only by acting as conduits of viral entry but also as reservoirs for productive and latent virus infection, and as producers of neurotoxins. Interaction between CX3CL1 (fractalkine) and FKN receptor (CX3CR1) is highly functional in the brain, and is known to regulate a complex network of paracrine and autocrine interactions between neurons and microglia. The aim of the present study was to determine which extent of HIV-1 Tat protein causes the alteration of CX3CR1 expression and to investigate the regulatory mechanism for CX3CR1 expression. Here we showed that exposure of primary microglia and BV2 cells to exogenous Tat protein resulted in down-regulation of CX3CR1 mRNA and protein expression, with a concomitant induction of proinflammatory responses. Next, we further showed that NF-κB activation by Tat treatment negatively regulated CX3CR1 expression. Since a YY1 binding site ~10kb upstream of CX3CR1 promoter was predicted in rats, mice and humans, the classical NF-κB-YY1 regulatory pathway was considered. Our findings indicated that Tat repressed CX3CR1 expression via NF-κB-YY1 regulatory pathway. To gain insight into the effect of Tat on CX3CL1-CX3CR1 communication, calcium mobilization, MAPK activation and microglial migration, respectively, were tested in microglial cells after successive treatment with Tat and CX3CL1. The results suggested that Tat disrupted the responses of microglia to CX3CL1. Taken together, these results demonstrate that HIV-1 Tat protein suppresses CX3CR1 expression in microglia via NF-κB-YY1 pathway and attenuates CX3CL1-induced functional response of microglia.
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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.