HIV-1 infection of macrophages differentially primes NK-cell cytotoxicity and proinflammatory cytokine production.

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^dim KIR+ and/or NKG2A+ NK cells. However, CD5

SUBMITTER: Mensching L 

PROVIDER: S-EPMC12268675 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature