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Toxins 2013, 5(9), 1629-1654; doi:10.3390/toxins5091629
Review

Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions

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)
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Abstract

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.
Keywords: staphylococcal superantigens; SEB; cytokine signaling; PI3K/mTOR; NFκB; FDA-approved drugs staphylococcal superantigens; SEB; cytokine signaling; PI3K/mTOR; NFκB; FDA-approved drugs
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Krakauer, T. Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions. Toxins 2013, 5, 1629-1654.

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