Toxicity of the staphylococcal enterotoxin B mutants with histidine-to-tyrosine substitutions

Evaluation of a Recombinant Double Mutant of Staphylococcal Enterotoxin B (SEB-H32Q/K173E) with Enhanced Antitumor Activity Effects and Decreased Pyrexia

“…However, several encouraging reports have indicated that there is no connection between adverse effects and the efficacy of T cell stimulation [19], [24]. Just as Korolev et al [20] proposed, we also confirmed that His 32 is an important residue that is closely related to SEB toxicity [25]. Therefore, we built the first MHC II-SEB-TCR ternary complex structural model to analyze the interaction between SEB and these receptors.…”

“…Previous studies have shown that emesis is not induced by SEB with carboxymethylated histidine residues [19]. Furthermore, Korolev et al [20] have shown that the substitution of histidine residues eliminates SEB toxicity while preserving its ability to induce T cell proliferation. These findings imply a lack of correlation between the biological activity and toxicity of SEB.…”

Comparative Opsonic and Protective Activities of Staphylococcus aureus Conjugate Vaccines Containing Native or Deacetylated Staphylococcal Poly- N -Acetyl-β-(1-6)-Glucosamine

“…S. aureus causes diverse infections such as endocarditis, septic arthritis, osteomyelitis, meningitis, skin infections, and abscesses (1,2,7,16,23,27) and there appears to be an increase in the recognition of community-acquired S. aureus infections, often involving methicillin-resistant S. aureus strains (16,27). It is now well appreciated that the emergence of antibiotic resistance among staphylococcal isolates has made the treatment of these infections increasingly difficult, which has amplified the call for new approaches to treat and prevent staphylococcal infections, such as immunotherapy.Ongoing efforts to design vaccines for S. aureus have targeted various virulence factors of this organism, including capsular polysaccharides (CP) (i.e., CP serotypes 5 and 8) (8, 9), cell wall-associated proteins (i.e., clumping factor A, fibronectin binding proteins, and collagen binding protein) (11,36,48), toxins (i.e., alpha-toxin, enterotoxins, and toxic shock syndrome toxin 1) (6,14,15,21,33), and the surface-associated polysaccharide, poly-N-acetyl-␤-(1-6)-glucosamine (PNAG) (25,26,29). PNAG is synthesized by enzymes encoded in the intercellular adhesin (ica) locus (12), which occurs not only in most clinical isolates of S. aureus but also in the majority of clinical isolates of CoNS (28,31,34,53), making PNAG an attractive vaccine candidate.…”

“…Ongoing efforts to design vaccines for S. aureus have targeted various virulence factors of this organism, including capsular polysaccharides (CP) (i.e., CP serotypes 5 and 8) (8, 9), cell wall-associated proteins (i.e., clumping factor A, fibronectin binding proteins, and collagen binding protein) (11,36,48), toxins (i.e., alpha-toxin, enterotoxins, and toxic shock syndrome toxin 1) (6,14,15,21,33), and the surface-associated polysaccharide, poly-N-acetyl-␤-(1-6)-glucosamine (PNAG) (25,26,29). PNAG is synthesized by enzymes encoded in the intercellular adhesin (ica) locus (12), which occurs not only in most clinical isolates of S. aureus but also in the majority of clinical isolates of CoNS (28,31,34,53), making PNAG an attractive vaccine candidate.…”

Staphylococcus aureus enterotoxin C2 mutants: biological activity assay in vitro

“…In addition, His118, is thought to correlate with emetic activity of SEs [15,23], and also was not essential for Tcell stimulation [5]. His-to-tyr substitution of SEB does not cause the conWrmation change and the mutant proteins retain the MHC-binding ability [11]. In this paper, for the Wrst time, we report that the mutated SEC2, obtained Jing Hui and Yan Cao have equal contribution.…”