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Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions

Department of Immunology, Integrated Toxicology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702 5011, USA
Toxins 2013, 5(9), 1629-1654; https://doi.org/10.3390/toxins5091629
Received: 8 July 2013 / Revised: 13 September 2013 / Accepted: 13 September 2013 / Published: 24 September 2013
(This article belongs to the Special Issue Enterotoxins: Microbial Proteins and Host Cell Dysregulation)
Staphylococcal enterotoxin B (SEB) and related bacterial toxins cause diseases in humans and laboratory animals ranging from food poisoning, acute lung injury to toxic shock. These superantigens bind directly to the major histocompatibility complex class II molecules on antigen-presenting cells and specific Vβ regions of T-cell receptors (TCR), resulting in rapid hyper-activation of the host immune system. In addition to TCR and co-stimulatory signals, proinflammatory mediators activate signaling pathways culminating in cell-stress response, activation of NFκB and mammalian target of rapamycin (mTOR). This article presents a concise review of superantigen-activated signaling pathways and focuses on the therapeutic challenges against bacterial superantigens. View Full-Text
Keywords: staphylococcal superantigens; SEB; cytokine signaling; PI3K/mTOR; NFκB; FDA-approved drugs staphylococcal superantigens; SEB; cytokine signaling; PI3K/mTOR; NFκB; FDA-approved drugs
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MDPI and ACS Style

Krakauer, T. Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions. Toxins 2013, 5, 1629-1654. https://doi.org/10.3390/toxins5091629

AMA Style

Krakauer T. Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions. Toxins. 2013; 5(9):1629-1654. https://doi.org/10.3390/toxins5091629

Chicago/Turabian Style

Krakauer, Teresa. 2013. "Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions" Toxins 5, no. 9: 1629-1654. https://doi.org/10.3390/toxins5091629

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