Enterotoxins: Microbial Proteins and Host Cell Dysregulation

© 2014 MDPI; under CC BY-NC-ND license

staphylococcal superantigens; SEB; cytokine signaling; PI3K/mTOR; NFκB; FDA-approved drugs; staphylococcal enterotoxin B; acute lung injury; hyaluronic acid; superantigen; staphylococcal enterotoxin B; MHC class II; T cell receptor; Clostridium perfringens; protein toxin; receptor; animal models; cell culture; vaccines; therapeutics; superantigens; yeast display; directed evolution; affinity maturation; T-cell receptor; complementarity determining regions; framework regions; Staphylococcal enterotoxin B; superantigen; food poisoning; Treg; gut-associated lymphoid tissue; intestinal inflammation; Staphylococcus aureus; toxic shock syndrome toxin-1; TNF-alpha; IL-2; neutralizing antibody; rabbit animal model; postexposure treatment; continual stimulation; Clostridium difficile toxin; domain interaction; autoprocessing; cytotoxicity; microscale thermophoresis; Clostridium; Bacillus; protein; binary enterotoxin; receptor; actin; Clostridium perfringens; beta-toxin; necrotizing enterocolitis; pore-forming toxin; staphylococcal enterotoxin B; inflammatory cytokines; sulfasalazine; Vibrio cholerae; cholera toxin B subunit; vaccine adjuvant; anti-inflammatory; clostridium perfringens enterotoxin; gynecologic cancer; Claudin; therapeutics; diagnostics; Clostridium perfringens type C; beta-toxin; endothelium; mucosa; epithelium; pathogenesis; porcine; shiga toxin; ribosome inactivating protein; P-protein stalk binding; sarcin/ricin loop depurination; superantigen; Staphylococcus aureus; nasal colonization; humanized mice; staphylococcal superantigens; clostridial toxins; receptor binding; toxicity; inflammation; therapeutics