ArticleJournal of immunology (Baltimore, Md. : 1950)2011
IFN-gamma mediates enhancement of HIV replication in astrocytes by inducing an antagonist of the beta-catenin pathway (DKK1) in a STAT 3-dependent manner.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 87 citations in OpenAlex.
- Modulation of mTOR, NLRP3, and Nrf2/HO-1 signaling by atorvastatin and nitazoxanide in experimental ulcerative colitis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epigenetic mechanisms of HIV and opioid-induced neuropathology: Potential therapies and interventions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- SARS-CoV-2 Infection Influences Wnt/β-Catenin Pathway Components in Astrocytes.Pathogens (Basel, Switzerland) · 2025Article
- The Complex Role of CD8+ T Cells in Placental HIV Infection.European journal of immunology · 2025Review
- Antiretroviral drug therapy does not reduce neuroinflammation in an HIV-1 infection brain organoid model.Journal of neuroinflammation · 2025Article
- Sociobehavioral Risk Factors and Clinical Implications of Late Presentation Among People Living with HIV in the Brazilian Amazon Region.AIDS and behavior · 2024Article
- RTCB deficiency triggers colitis in mice by influencing the NF-κB and Wnt/β-catenin signaling pathways.Acta biochimica et biophysica Sinica · 2024Article
- Involvement of DKK1 secreted from adipose-derived stem cells in alopecia areata.Cell proliferation · 2024Article
- Ascorbate protects human kidney organoids from damage induced by cell-free hemoglobin.Disease models & mechanisms · 2023Article
- Astrocytes and the Psychiatric Sequelae of COVID-19: What We Learned from the Pandemic.Neurochemical research · 2023Review
- HIV infection of non-classical cells in the brain.Retrovirology · 2023Review
- Anxiety, depression, and memory loss in Chagas disease: a puzzle far beyond neuroinflammation to be unpicked and solved.Memorias do Instituto Oswaldo Cruz · 2023Article
- Dickkopf proteins in pathological inflammatory diseases.Journal of leukocyte biology · 2022Review
- Neuroinflammation in Schizophrenia: The Key Role of the WNT/β-Catenin Pathway.International journal of molecular sciences · 2022Review
- Mini-review: The therapeutic role of cannabinoids in neuroHIV.Neuroscience letters · 2021Review
- The far-reaching HAND of cART: cART effects on astrocytes.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Review
- Systemic Inflammation and Astrocyte Reactivity in the Neuropsychiatric Sequelae of COVID-19: Focus on Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2021Article
- Article
- Alzheimer's disease-like perturbations in HIV-mediated neuronal dysfunctions: understanding mechanisms and developing therapeutic strategies.Open biology · 2020Review
- Targeting Cannabinoid Receptor 2 on Peripheral Leukocytes to Attenuate Inflammatory Mechanisms Implicated in HIV-Associated Neurocognitive Disorder.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Typically, IFN-γ is an antiviral cytokine that inhibits the replication of many viruses, including HIV. However, in the CNS, IFN-γ induces HIV-productive replication in astrocytes. Although astrocytes in vitro are refractory to HIV replication, recent in vivo evidence demonstrated that astrocytes are infected by HIV, and their degree of infection is correlated with proximity to activated macrophages/microglia. The ability of IFN-γ to induce HIV replication in astrocytes suggests that the environmental milieu is critical in regulating the permissiveness of astrocytes to HIV infection. We evaluated the mechanism by which IFN-γ relieves restricted HIV replication in astrocytes. We demonstrate that although astrocytes have robust endogenous β-catenin signaling, a pathway that is a potent inhibitor of HIV replication, IFN-γ diminished β-catenin signaling in astrocytes by 40%, as evaluated by both active β-catenin protein expression and β-catenin-mediated T cell factor/lymphoid enhancer reporter (TOPflash) activity. Further, IFN-γ-mediated inhibition of β-catenin signaling was dependent on its ability to induce an antagonist of the β-catenin signaling pathway, Dickkopf-related protein 1, in a STAT 3-dependent manner. Inhibition of STAT3 and Dickkopf-related protein 1 abrogated the ability of IFN-γ to enhance HIV replication in astrocytes. These data demonstrated that IFN-γ induces HIV replication in astrocytes by antagonizing the β-catenin pathway. To our knowledge, this is the first report to point to an intricate cross-talk between IFN-γ signaling and β-catenin signaling that may have biologic and virologic effects on HIV outcome in the CNS, as well as on broader processes where the two pathways interface.
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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.