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The staphylococcal enterotoxins and their relatives.

P Marrack¹, J Kappler

¹Howard Hughes Medical Institute, Department of Medicine, Denver, CO.

Science (New York, N.Y.)

|May 11, 1990

Summary

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.

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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.

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