ArticlePLoS pathogens2017
The Staphylococcus aureus superantigen SElX is a bifunctional toxin that inhibits neutrophil function.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- Dual-Scale StaphAIR: Predictive Modeling for the Diagnosis ofAnalytical chemistry · 2026Article
- Immune evasion of multidrug-resistant bacteria: insights from lung innate immune cells and targeted therapies.Frontiers in cellular and infection microbiology · 2026Review
- Novel insights into the immune response to bacterial T cell superantigens.Nature reviews. Immunology · 2024Review
- History of S. aureus Skin Infection Significantly Associates with History of Eczema Herpeticum in Patients with Atopic Dermatitis.Dermatology and therapy · 2023Article
- Staphylococcus aureus host interactions and adaptation.Nature reviews. Microbiology · 2023Review
- Local, systemic and immunologic safety comparison between xenogeneic equine umbilical cord mesenchymal stem cells, allogeneic canine adipose mesenchymal stem cells and placebo: a randomized controlled trial.Frontiers in veterinary science · 2023Article
- Enterotoxin Gene Cluster andCells · 2022Article
- Superantigens, a Paradox of the Immune Response.Toxins · 2022Review
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- Staphylococcus lugdunensis Uses the Agr Regulatory System to Resist Killing by Host Innate Immune Effectors.Infection and immunity · 2022Article
- SEC is an antiangiogenic virulence factor that promotesScience advances · 2022Article
- Multiple Domains of Staphylococcal Superantigen-like Protein 11 (SSL11) Contribute to Neutrophil Inhibition.Biochemistry · 2022Article
- Superantigens promoteProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Molecular docking and proteomics reveals the synergistic antibacterial mechanism of theaflavin with β-lactam antibiotics against MRSA.Frontiers in microbiology · 2022Article
- Pathogenicity and virulence ofVirulence · 2021Review
- Review
- Sialoglycan recognition is a common connection linking acidosis, zinc, and HMGB1 in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Toxic Shock Syndrome Toxin 1 Induces Immune Response via the Activation of NLRP3 Inflammasome.Toxins · 2021Article
- Superantigen Recognition and Interactions: Functions, Mechanisms and Applications.Frontiers in immunology · 2021Review
- Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Bacterial superantigens (SAgs) cause Vβ-dependent T-cell proliferation leading to immune dysregulation associated with the pathogenesis of life-threatening infections such as toxic shock syndrome, and necrotizing pneumonia. Previously, we demonstrated that staphylococcal enterotoxin-like toxin X (SElX) from Staphylococcus aureus is a classical superantigen that exhibits T-cell activation in a Vβ-specific manner, and contributes to the pathogenesis of necrotizing pneumonia. Here, we discovered that SElX can also bind to neutrophils from human and other mammalian species and disrupt IgG-mediated phagocytosis. Site-directed mutagenesis of the conserved sialic acid-binding motif of SElX abolished neutrophil binding and phagocytic killing, and revealed multiple glycosylated neutrophil receptors for SElX binding. Furthermore, the neutrophil binding-deficient mutant of SElX retained its capacity for T-cell activation demonstrating that SElX exhibits mechanistically independent activities on distinct cell populations associated with acquired and innate immunity, respectively. Finally, we demonstrated that the neutrophil-binding activity rather than superantigenicity is responsible for the SElX-dependent virulence observed in a necrotizing pneumonia rabbit model of infection. Taken together, we report the first example of a SAg, that can manipulate both the innate and adaptive arms of the human immune system during S. aureus pathogenesis.
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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 OpenQuestion graph.