ArticleProceedings of the National Academy of Sciences of the United States of America2016
Superantigens hyperinduce inflammatory cytokines by enhancing the B7-2/CD28 costimulatory receptor interaction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 60 citations in OpenAlex.
- NKG2A-mediated immune modulation of natural killer cells by Staphylococcus aureus.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A superantigen-based MHC class II-targeted cancer immunotherapy for the treatment of acute myeloid leukemia.Blood cancer journal · 2025Article
- A highly neutralizing human monoclonal antibody targeting a novel linear epitope on staphylococcal enterotoxin B.Human vaccines & immunotherapeutics · 2024Article
- Botensilimab, an Fc-Enhanced Anti-CTLA-4 Antibody, Is Effective against Tumors Poorly Responsive to Conventional Immunotherapy.Cancer discovery · 2024Article
- Staphylococcal superantigens evoke temporary and reversible T cell anergy, but fail to block the development of a bacterium specific cellular immune response.Nature communications · 2024Article
- Subduing the Inflammatory Cytokine Storm.International journal of molecular sciences · 2024Review
- High-Affinity Superantigen-Based Trifunctional Immune Cell Engager Synergizes NK and T Cell Activation for Tumor Suppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Novel insights into the immune response to bacterial T cell superantigens.Nature reviews. Immunology · 2024Review
- Enhanced CD95 and interleukin 18 signalling accompany T cell receptor Vβ21.3+ activation in multi-inflammatory syndrome in children.Nature communications · 2024Article
- Review
- Fc gamma receptors promote antibody-induced LILRB4 internalization and immune regulation of monocytic AML.Antibody therapeutics · 2024Article
- Blocking Superantigen-Mediated Diseases: Challenges and Future Trends.Journal of immunology research · 2024Review
- Targeting staphylococcal enterotoxin B binding to CD28 as a new strategy for dampening superantigen-mediated intestinal epithelial barrier dysfunctions.Frontiers in immunology · 2024Article
- The homodimer interfaces of costimulatory receptors B7 and CD28 control their engagement and pro-inflammatory signaling.Journal of biomedical science · 2023Article
- The superantigens SpeC and TSST-1 specifically activate TRBV12-3/12-4Communications biology · 2023Article
- Bivalent binding of staphylococcal superantigens to the TCR and CD28 triggers inflammatory signals independently of antigen presenting cells.Frontiers in immunology · 2023Article
- Superantigens, a Paradox of the Immune Response.Toxins · 2022Review
- Article
- Generation and expression analysis of BAC humanized mice carrying HLA-DP401 haplotype.Animal models and experimental medicine · 2021Article
- Bystander Memory T Cells and IMiD/Checkpoint Therapy in Multiple Myeloma: A Dangerous Tango?Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Full T-cell activation requires interaction between the costimulatory receptors B7-2 and CD28. By binding CD28, bacterial superantigens elicit harmful inflammatory cytokine overexpression through an unknown mechanism. We show that, by engaging not only CD28 but also its coligand B7-2 directly, superantigens potently enhance the avidity between B7-2 and CD28, inducing thereby T-cell hyperactivation. Using the same 12-aa β-strand-hinge-α-helix domain, superantigens engage both B7-2 and CD28 at their homodimer interfaces, areas remote from where these coreceptors interact, implying that inflammatory signaling can be controlled through the receptor homodimer interfaces. Short B7-2 dimer interface mimetic peptides bind diverse superantigens, prevent superantigen binding to cell-surface B7-2 or CD28, attenuate inflammatory cytokine overexpression, and protect mice from lethal superantigen challenge. Thus, superantigens induce a cytokine storm not only by mediating the interaction between MHC-II molecule and T-cell receptor but also, critically, by promoting B7-2/CD28 coreceptor engagement, forcing the principal costimulatory axis to signal excessively. Our results reveal a role for B7-2 as obligatory receptor for superantigens. B7-2 homodimer interface mimotopes prevent superantigen lethality by blocking the superantigen-host costimulatory receptor interaction.
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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.