期刊
FRONTIERS IN IMMUNOLOGY
卷 14, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2023.1170821
关键词
staphylococcal superantigens; T cells; TCR (T cell receptor); CD28; inflammation
类别
Staphylococcus aureus superantigens (SAgs) like staphylococcal enterotoxin A (SEA) and B (SEB) can cause toxic shock and sepsis by stimulating T cells to produce excessive inflammatory cytokines. Using an AI-based algorithm, we have discovered a new mechanism of action for SAgs, showing that SEA and SEB can bind to TCR and CD28 independently of MHC class II- and B7-expressing antigen presenting cells, leading to inflammatory signal activation and massive cytokine secretion.
Staphylococcus aureus superantigens (SAgs) such as staphylococcal enterotoxin A (SEA) and B (SEB) are potent toxins stimulating T cells to produce high levels of inflammatory cytokines, thus causing toxic shock and sepsis. Here we used a recently released artificial intelligence-based algorithm to better elucidate the interaction between staphylococcal SAgs and their ligands on T cells, the TCR and CD28. The obtained computational models together with functional data show that SEB and SEA are able to bind to the TCR and CD28 stimulating T cells to activate inflammatory signals independently of MHC class II- and B7-expressing antigen presenting cells. These data reveal a novel mode of action of staphylococcal SAgs. By binding to the TCR and CD28 in a bivalent way, staphylococcal SAgs trigger both the early and late signalling events, which lead to massive inflammatory cytokine secretion.
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