ArticleiScience2025
HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Targeting HIV myeloid and central nervous system reservoirs for HIV cure.Current opinion in HIV and AIDS · 2025Review
- A transatlantic joint lab model for interdisciplinary research.Nature microbiology · 2025Article
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Natural killer (NK) cells are innate cytotoxic lymphocytes with antiviral functions explored in "shock and kill" strategies to eliminate the HIV-1 reservoir. For optimal activity against infected targets, NK cells require priming. This study examined how macrophages prime NK cells following HIV-1 infection. We found that HIV-1-infected monocyte-derived macrophages upregulated membrane-bound IL-15Rα, NKG2D ligands, CD48, and IL-18. While crosstalk between NK cells and infected macrophages enhanced proinflammatory cytokine production, it led to only weak priming of NK-cell cytotoxicity. In people living with HIV-1 (PLWH) on antiretroviral therapy, macrophage priming remained intact and polyfunctional, with the strongest response in CD56
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