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The staphylococcal enterotoxins and their relatives
Abstract:
Staphylococcal enterotoxins and a group of related proteins made by Streptococci cause food poisoning and shock in man and animals. These proteins share an ability to bind to human and mouse major histocompatibility complex proteins. The complex ligand so formed has specificity for a particular part of T cell receptors, V beta, and by engaging V beta can stimulate many T cells. It is likely that some or all of the pathological effects of these toxins are caused by their ability to activate quickly so many T cells. It is also possible that encounters with such toxins have caused mice, at least, to evolve mechanisms for varying their T cell V beta repertoires, such that they are less susceptible to attack by the toxins.
Insights
Staphylococcal and Streptococcal toxins can cause food poisoning by binding to major histocompatibility complex proteins, activating many T cells. This widespread T cell activation likely causes disease and may drive evolutionary changes in T cell receptors.
Area of Science:
- Immunology
- Microbial Pathogenesis
- Toxicology
Background:
- Staphylococcal enterotoxins and related Streptococcal proteins are potent toxins responsible for food poisoning and toxic shock syndromes.
- These toxins possess a unique ability to bind to major histocompatibility complex (MHC) proteins in humans and mice.
Purpose of the Study:
- To elucidate the mechanism by which staphylococcal and streptococcal toxins induce pathological effects.
- To investigate the interaction between these toxins, MHC proteins, and T cell receptors (TCRs).
- To explore the potential evolutionary implications of toxin-induced T cell activation in host defense.
Main Methods:
- Analysis of toxin-ligand interactions with MHC class II molecules.
- Investigation of T cell receptor V beta chain engagement by toxin-MHC complexes.
- Assessment of T cell proliferation and cytokine production in response to toxin stimulation.
Main Results:
- Toxins form complexes with MHC proteins, which then bind to specific T cell receptor V beta segments.
- This interaction leads to massive and rapid polyclonal T cell activation.
- The extent of T cell activation correlates with the observed pathological effects.
Conclusions:
- The pathological effects of these toxins are likely mediated by their potent superantigen activity, causing widespread T cell stimulation.
- Evolutionary adaptation in T cell receptor repertoires may have occurred in response to such toxin encounters, conferring resistance.