ArticleNature communications2024
Staphylococcal superantigens evoke temporary and reversible T cell anergy, but fail to block the development of a bacterium specific cellular immune response.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- Convergent evolution of immune evasion in ESKAPE pathogens: A cross-pathogen architecture of conserved host-defense checkpoints.European journal of microbiology & immunology · 2026Review
- The Impact of Severe Albuminuria on the Proinflammatory Monocyte Subset CD14++CD16+ and Antigen-Specific Immune Responses.International journal of molecular sciences · 2026Article
- Transcriptomic profiling of TSST-1-induced cytotoxicity and inflammatory responses in human vaginal epithelial cells.BMC microbiology · 2026Article
- Companion animals as potentially important reservoir of methicillin-resistant and virulent strains of coagulase-positive Staphylococcus spp.BMC veterinary research · 2026Article
- Multivalent nanobodies for potent and broad neutralization of Staphylococcus aureus toxins.Nature communications · 2026Article
- Identifying Cytokine Motif-Containing, Immunomodulatory Bacterial Proteins in Human Gut Microbiome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Acquisition of toxin-encoding lysogenic bacteriophage elements enhances the virulence of pandemicInfection and immunity · 2026Article
- Antibacterial Immunotherapy: Mechanistic Insights, Emerging Therapeutic Strategies, and Clinical Translation.Infection and drug resistance · 2026Review
- Cell-intrinsic CD4 T cell tolerance: a new frontier in therapy?Trends in immunology · 2025Review
- The lack of a biorepository during vaccine trials: A lost opportunity to understand staphylococcal immunity.Vaccine · 2025Article
- A potential XGBoost Diagnostic Score forFrontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Superantigens (sAgs) are bacterial virulence factors that induce a state of immune hyperactivation by forming a bridge between certain subsets of T cell receptor (TCR) β chains on T lymphocytes, and class II major histocompatibility complex (MHC-II) molecules; this cross-linking leads to indiscriminate T cell activation, cytokine storm and toxic shock. Here we show that sAg exposure drives the preferential expansion of naive and central memory T cell subsets, but not effector or resident memory T cells, which instead, hyper release pro-inflammatory cytokines. A targeted therapeutic approach to minimise cytokine release by effector memory T cells attenuated sAg-induced cytokine release. Irrespective of antigen experience, sAg activation does not render mature T cells permanently dysfunctional, and full restoration of effector function is observed following a transient and reversible anergy. Moreover, we show that in the face of sAg induced immune hyperactivation, an intact bacterium-specific CD4
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