ArticleJournal of immunology (Baltimore, Md. : 1950)2023
HIV-1 Tat Upregulates TREM1 Expression in Human Microglia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- HIV gp120 induces TREM1 expression through TLR-PGE₂ signalling in human monocyte-derived microglia.Journal of neuroinflammation · 2026Article
- Decoding cross-talk between Mpox and HIV: insights from transcriptomics and network-based analyses.Virology journal · 2025Article
- Targeting HIV myeloid and central nervous system reservoirs for HIV cure.Current opinion in HIV and AIDS · 2025Review
- The Role and Mechanism of TRIM13 Regulation of TRAF6 Ubiquitination in the Synergy of Inflammatory Responses and Neurotoxicity Induced by METH and HIV- 1 Tat Protein in Astrocytes.Neurotoxicity research · 2025Article
- The properties of TREM1 and its emerging role in pain-related diseases.Molecular brain · 2025Review
- Viral reprogramming of glial metabolism as a driver of neuroinflammation.Frontiers in immunology · 2025Review
- Article
- Neurological impact of HIV/AIDS and substance use alters brain function and structure.Frontiers in medicine · 2024Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Because microglia are a reservoir for HIV and are resistant to the cytopathic effects of HIV infection, they are a roadblock for any HIV cure strategy. We have previously identified that triggering receptor expressed on myeloid cells 1 (TREM1) plays a key role in human macrophage resistance to HIV-mediated cytopathogenesis. In this article, we show that HIV-infected human microglia express increased levels of TREM1 and are resistant to HIV-induced apoptosis. Moreover, upon genetic inhibition of TREM1, HIV-infected microglia undergo cell death in the absence of increased viral or proinflammatory cytokine expression or the targeting of uninfected cells. We also show that the expression of TREM1 is mediated by HIV Tat through a TLR4, TICAM1, PG-endoperoxide synthase 2, PGE synthase, and PGE2-dependent manner. These findings highlight the potential of TREM1 as a therapeutic target to eradicate HIV-infected microglia without inducing a proinflammatory response.
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What Socratic 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 Socratic graph.