Abstract
Staphylococcal exotoxins (SE) are among the most common etiological agents that cause toxic shock (1). Similar to other superantigens, SE activates T cells polyclonally by binding simultaneously to specific Vβ regions of T-cell receptors (TCR) on T cells and the major histocompatibility complex class II (MHC II) molecules on antigen-presenting cells (APCs) (2,3). Interaction of SE with TCR and MHC II results in a massive release of proinflammatory cytokines from stimulated cells (4,5). Previous studies demonstrated that the cytokines produced, tumor-necrosis factor (TNF-α), interleukin 1 (IL-1), and interferon-γ (IFN-γ) are pivotal mediators in SE-induced toxic shock (6,7). High levels of these cytokines in serum are pathogenic and correlate with clinical symptoms of toxic shock (8,10).
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Krakauer, T., Chen, X., Zack Howard, O.M., Young, H.A. (2003). RNase Protection Assay for the Study of the Differential Effects of Therapeutic Agents in Suppressing Staphylococcal Enterotoxin B-Induced Cytokines in Human Peripheral Blood Mononuclear Cells. In: Krakauer, T. (eds) Superantigen Protocols. Methods in Molecular Biology™, vol 214. Humana Press. https://doi.org/10.1385/1-59259-367-4:151
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DOI: https://doi.org/10.1385/1-59259-367-4:151
Publisher Name: Humana Press
Print ISBN: 978-0-89603-984-1
Online ISBN: 978-1-59259-367-5
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