Superantigen peptide antagonists failed to block T-cell activation and cytokine production as well as toxic shock induced by staphylococcal enterotoxin B (SEB) in HLA class II transgenic mice. They also failed to inhibit the binding of SEB to HLA class II molecules as well as activation of human T lymphocytes in vitro.

background rheumatoid arthritis (ra) is the most common chronic inflammatory disease of unknown etiology. in this regard, the role of bacterial superantigens (as an effective agent) were considered. objectives this study aimed to assess staphylococcal enterotoxin e in the blood of patients with rheumatoid arthritis. patients and methods a total of 83 blood samples of patients with ra were studi...

To study the major histocompatibility complex class II I-E dependence of mouse mammary tumor virus (MMTV) superantigens, we constructed hybrids between the I-E-dependent MMTV(GR) and the I-E-independent mtv-7 superantigens and tested them in vivo. Our results suggest that, although the C-terminal third mediates I-A interaction, additional binding sites are located elsewhere in the superantigen.

We investigated the biological properties of a novel staphylococcal enterotoxin-like putative toxin, staphylococcal enterotoxin-like toxin type R (SElR). Major histocompatibility complex class II molecules were required for T-cell stimulation by SElR. SElR stimulated T cells bearing receptors Vbeta 3, 11, 12, 13.2, and 14. These results suggested that SElR acts as a superantigen.

We obtained a draft genome sequence of Staphylococcus aureus strain S54F9, which was isolated from a chronic disseminated porcine lung abscess and used in porcine infection models. Genes coding for a number of toxins, including enterotoxins and superantigen, were demonstrated in this strain.