Enterotoxin type B Protein, S. aureus (P.pastoris, His)

Enterotoxin type B, S. aureus is a superantigen of enterotoxin B (SEB) derived from Staphylococcus aureus (S. aureus), which belongs to the staphylococcal enterotoxin family. Enterotoxin B structurally binds to MHC class II molecules on antigen presenting cells and binds to the variable region of the β chain of the T cell receptor (TCR), activating T cells expressing a specific (Vβ)-TCR fragment. Enterotoxin B-TCR triggers massive activation of CD4+ and CD8+ T cells, leading to the release of proinflammatory cytokines (TNF-α, IFN-γ) and Th2-type cytokines (IL-4, IL-5, IL-13), and mediates the synthesis of nitric oxide (NO) through TNF and IFN-γ. The activity of enterotoxin B involves a regulatory loop in which NO downregulates cytokine production to prevent excessive inflammation. Enterotoxin B has been shown to induce T_H2-biased cytokine release in a nasal polyp model; in an endotoxin shock model, NO-mediated protection against lethal cytokine storm was observed. In addition, intravenous administration of Enterotoxin B enhanced IFN-γ production and CD4+/CD8+ T cell infiltration, demonstrated anti-tumor potential in a fibrosarcoma model, and induced tumor necrosis.

Enterotoxin type B Protein, S. aureus (100 μg; intraperitoneal injection; 1 time; single dose) can induce a large amount of NO synthesis in the mouse endotoxin shock model. The synthesis of NO is regulated by TNF and IFN-γ. At the same time, endogenous NO can downregulate the production of TNF and IFN-γ and play a protective role. Inhibition of NO synthesis will lead to the death of mice, while neutralization of IFN-γ and TNF can reduce the mortality of mice^[1].
Enterotoxin type B Protein, S. aureus (10 ng; intravenous injection; once every 3 days; 2 weeks) can significantly inhibit the tumor growth of the mouse fibrosarcoma model, increase the IFN-γ level and CD4+/CD8+ T cell infiltration rate, and induce tumor tissue necrosis, while intratumoral injection has no obvious tumor inhibition effect^[2].