Staphylococcal and streptococcal superantigen exotoxins

Abstract

SUMMARY This review begins with a discussion of the large family of Staphylococcus aureus and beta-hemolytic streptococcal pyrogenic toxin T lymphocyte superantigens from structural and immunobiological perspectives. With this as background, the review then discusses the major known and possible human disease associations with superantigens, including associations with toxic shock syndromes, atopic dermatitis, pneumonia, infective endocarditis, and autoimmune sequelae to streptococcal illnesses. Finally, the review addresses current and possible novel strategies to prevent superantigen production and passive and active immunization strategies.

Fig 1

Three-dimensional structure of the group I superantigen TSST-1. Light blue, low-affinity MHC II binding site; red, Vβ-TCR binding site; yellow, epithelial/endothelial/CD40/CD28 binding site.

Fig 2

Three-dimensional structure of the group III superantigen SEA. Light blue, low-affinity MHC II binding site; dark blue, high-affinity MHC II binding site; red, Vβ-TCR binding site; white, emetic cystine loop; yellow, epithelial/endothelial/CD40/CD28 binding site.

Fig 3

Model for S. aureus production of pneumonia. The presence of S. aureus in the lungs leads to inflammation due to alpha-toxin and superantigens and to TSS due to superantigens, both leading to anoxia, hypotension, and possibly death.

Fig 4

Model of possible roles of S. aureus superantigens in infective endocarditis. S. aureus may colonize damaged endothelium of heart valves (A) and, through combinations of superantigenicity (immune dysfunction), superantigen-induced failure of endothelium healing (maintenance of endothelial damage), and induction of capillary leakage, may facilitate vegetation formation (B).