ArticleJournal of immunology (Baltimore, Md. : 1950)2025
NKG2A-mediated immune modulation of natural killer cells by Staphylococcus aureus.
Article in Journal of immunology (Baltimore, Md. : 1950), 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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Who cites it
2 citing papers in PubMed.
- NK Cell Disfunction in Atopic Dermatitis: A Missing Link Between Type 2 Inflammation, Microbial Dysbiosis and Antiviral Immunity.International journal of molecular sciences · 2026Review
- Modulation of NK Cell Properties by ESKAPE Group Bacteria.International journal of molecular sciences · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Natural killer (NK) cells are specialized lymphocytes that help protect against viruses and cancer. However, in the context of bacterial infections, NK cells can be harmful, rather than protective. Such immune pathogenesis by NK cells has been linked to the overproduction of proinflammatory cytokines like interferon-gamma (IFN-γ). In this context, IFN-γ-deficient mice display increased survival rates in response to Staphylococcus aureus (S. aureus) infection. However, little is known about how NK cells respond to S. aureus in humans, which causes life-threatening, invasive systemic infections with high mortality rates. In this study, we found that the peripheral blood of patients with bloodstream S. aureus infection was enriched for CD57- NKG2A+ NK cells with greater cytokine-producing capacity, compared to healthy controls and those hospitalized with Escherichia coli bloodstream infections. As a possible mechanistic cause, superantigens from S. aureus promoted the expansion of CD57- NKG2A+ NK cells that produced IFN-γ through a mechanism that appears to be IL-12 independent and exhibited reduced levels of CD16 compared to unstimulated NK cells. These data suggest that S. aureus bloodstream infection in humans promotes a phenotypic shift toward CD57- NKG2A+ NK cells with greater IFN-γ-producing capacity, providing a plausible way to promote inflammation-driven disease pathogenesis.
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Registered trials
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