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Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions

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...

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Autor principal: Krakauer, Teresa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798877/
https://www.ncbi.nlm.nih.gov/pubmed/24064719
http://dx.doi.org/10.3390/toxins5091629
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author Krakauer, Teresa
author_facet Krakauer, Teresa
author_sort Krakauer, Teresa
collection PubMed
description 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.
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spelling pubmed-37988772013-10-21 Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions Krakauer, Teresa Toxins (Basel) Article 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. MDPI 2013-09-24 /pmc/articles/PMC3798877/ /pubmed/24064719 http://dx.doi.org/10.3390/toxins5091629 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Krakauer, Teresa
Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title_full Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title_fullStr Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title_full_unstemmed Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title_short Update on Staphylococcal Superantigen-Induced Signaling Pathways and Therapeutic Interventions
title_sort update on staphylococcal superantigen-induced signaling pathways and therapeutic interventions
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3798877/
https://www.ncbi.nlm.nih.gov/pubmed/24064719
http://dx.doi.org/10.3390/toxins5091629
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