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Bivalent binding of staphylococcal superantigens to the TCR and CD28 triggers inflammatory signals independently of antigen presenting cells. | LitMetric

AI Article Synopsis

  • Superantigens like staphylococcal enterotoxins A and B (SEA and SEB) are powerful toxins that can cause toxic shock and sepsis by activating T cells to produce a large amount of inflammatory cytokines.
  • A new AI-based algorithm was used to study how these superantigens interact with the T cell receptors (TCR) and CD28, showing that SEA and SEB can stimulate T cells without relying on antigen presenting cells.
  • The findings suggest that superantigens bind to TCR and CD28 in a unique way, triggering both early and late signaling that results in a significant increase in inflammatory cytokine secretion.

Article Abstract

s 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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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10189049PMC
http://dx.doi.org/10.3389/fimmu.2023.1170821DOI Listing

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