1992
DOI: 10.1111/j.1365-2249.1992.tb02995.x
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Involvement of HLA class II molecules in acquisition of staphylococcal enterotoxin A-binding activity and accessory cell activity in activation of human T cells by related toxins in vascular endothelial cells

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Cited by 12 publications
(3 citation statements)
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References 34 publications
(23 reference statements)
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“…Furthermore, SAgs trigger cytokine release from activated APCs via MHC class II and mucosal cell barrier disruption [26,27]. Clinically, SAgs result in hypotension by binding directly to MHC class II on endothelial cells which then interact with SEB or TSST-1 and cause the release of vasoactive mediators such as tumor necrosis factor-alpha (TNF-α) from host leukocytes [28][29][30]. In the present study, we address SFP and TSS caused by SEs and TSST-1, respectively, although SAgs have been implicated in the pathogenesis of a various human diseases including Kawasaki disease, atopic dermatitis and airway allergies [14,31,32].…”
Section: Staphylococcus Aureus Toxins: Basic Concepts Of Their Pathogmentioning
confidence: 99%
“…Furthermore, SAgs trigger cytokine release from activated APCs via MHC class II and mucosal cell barrier disruption [26,27]. Clinically, SAgs result in hypotension by binding directly to MHC class II on endothelial cells which then interact with SEB or TSST-1 and cause the release of vasoactive mediators such as tumor necrosis factor-alpha (TNF-α) from host leukocytes [28][29][30]. In the present study, we address SFP and TSS caused by SEs and TSST-1, respectively, although SAgs have been implicated in the pathogenesis of a various human diseases including Kawasaki disease, atopic dermatitis and airway allergies [14,31,32].…”
Section: Staphylococcus Aureus Toxins: Basic Concepts Of Their Pathogmentioning
confidence: 99%
“…An example of the degranulation of mast cells, it may be triggered by SEs via direct binding to receptors on these cells rather than through the typical immunoglobulin E-mediated process of mast cell activation [91]. Further, MHC class II molecules have been implicated as the receptors on endothelial cells that interact with TSST-1 or SEB [92][93][94]. SEB, in addition, caused barrier dysfunction and cytotoxic injury to monolayers of bovine or human pulmonary artery endothelial cells [95].…”
Section: Ptsags Family Of Exotoxinsmentioning
confidence: 99%
“…Based on antigenic heterogeneity, more than 20 SEs (SEA-SElV) have been discovered [81,84,85]. Although the receptors involved in the emetic response to SEs have not been discovered, clinical signs of SFP have been linked to inflammatory mediators, such as leukotriene B4 and prostaglandin E2, both of which are produced in response to SEs [86,87]. The stomach and upper small intestine present the most significant mucosa lesions, which are associated with neutrophil infiltrates in the epithelium and lamina propria, whereas the jejunum exhibits broken brush boundaries and enlarged crypts [88].…”
Section: Staphylococcal Enterotoxins (Ses)mentioning
confidence: 99%