ArticleThe Journal of clinical investigation2024
Pathobiont-driven antibody sialylation through IL-10 undermines vaccination.
Article in The Journal of clinical investigation, 2024. 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.
- Methicillin-resistant and susceptible Staphylococcus aureus: tolerance, immune evasion and treatment.Nature reviews. Microbiology · 2026Review
- ESAT-6 and CFP-10 reactive IgG in patients with tuberculosis inhibits intracellular bacteria.Cell reports · 2025Article
- Synthesis, Conformal Analysis, and Antibody Binding of Staphylococcus aureus Capsular Polysaccharide Type 5 Oligosaccharides.Angewandte Chemie (International ed. in English) · 2025Article
- Article
- Article
- The lack of a biorepository during vaccine trials: A lost opportunity to understand staphylococcal immunity.Vaccine · 2025Article
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
- IL-10 and IL-2R as combined predictors of intravenous immunoglobulin resistance in Kawasaki disease: a retrospective cohort study.Frontiers in immunology · 2025Article
- Interleukin 10 drives Staphylococcus aureus imprinting and vaccine failure in murine models via antibody glycosylation.The Journal of clinical investigation · 2024Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
The pathobiont Staphylococcus aureus (Sa) induces nonprotective antibody imprints that underlie ineffective staphylococcal vaccination. However, the mechanism by which Sa modifies antibody activity is not clear. Herein, we demonstrate that IL-10 is the decisive factor that abrogates antibody protection in mice. Sa-induced B10 cells drive antigen-specific vaccine suppression that affects both recalled and de novo developed B cells. Released IL-10 promotes STAT3 binding upstream of the gene encoding sialyltransferase ST3gal4 and increases its expression by B cells, leading to hyper-α2,3sialylation of antibodies and loss of protective activity. IL-10 enhances α2,3sialylation on cell-wall-associated IsdB, IsdA, and MntC antibodies along with suppression of the respective Sa vaccines. Consistent with mouse findings, human anti-Sa antibodies as well as anti-pseudomonal antibodies from cystic fibrosis subjects (high IL-10) are hypersialylated, compared with anti-Streptococcus pyogenes and pseudomonal antibodies from normal individuals. Overall, we demonstrate a pathobiont-centric mechanism that modulates antibody glycosylation through IL-10, leading to loss of staphylococcal vaccine efficacy.
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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 Socratic graph.