pi3kaktmtor, a pathway less recognized for staphylococcal superantigen-induced toxicity的途径少承认pi3kaktmtor葡萄球菌superantigen-induced毒性.pdfVIP

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pi3kaktmtor, a pathway less recognized for staphylococcal superantigen-induced toxicity的途径少承认pi3kaktmtor葡萄球菌superantigen-induced毒性.pdf

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pi3kaktmtor, a pathway less recognized for staphylococcal superantigen-induced toxicity的途径少承认pi3kaktmtor葡萄球菌superantigen-induced毒性

Toxins 2012, 4, 1343-1366; doi:10.3390/toxins4111343 OPEN ACCESS toxins ISSN 2072-6651 /journal/toxins Review PI3K/Akt/mTOR, a Pathway Less Recognized for Staphylococcal Superantigen-Induced Toxicity Teresa Krakauer Department of Immunology, Integrated Toxicology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD 21702, USA; E-Mail: teresa.krakauer@; Tel.: +1-301-619-4733; Fax: +1-301-619-2348 Received: 27 September 2012; in revised form: 12 November 2012 / Accepted: 13 November 2012 / Published: 15 November 2012 Abstract: Immunostimulating staphylococcal enterotoxin B (SEB) and related superantigenic toxins cause diseases in humans and laboratory animals by activating cells of the immune system. These toxins bind directly to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and specific Vβ regions of T-cell receptors (TCR), resulting in hyperactivation of both T lymphocytes and monocytes/macrophages. Activated host cells produce excessive amounts of proinflammatory cytokines and chemokines, especially tumor necrosis factor α, interleukin 1 (IL-1), IL-2, interferon γ (IFNγ), and macrophage chemoattractant protein 1 causing clinical symptoms of fever, hypotension, and shock. The well-explored signal transduction pathways for SEB-induced toxicity downstream from TCR/MHC ligation and interaction