Journal
ANNUAL REVIEW OF MICROBIOLOGY
Volume 55, Issue -, Pages 77-104Publisher
ANNUAL REVIEWS
DOI: 10.1146/annurev.micro.55.1.77
Keywords
Staphylococcus aureus; Streptococcus pyogenes; hypotension; T cell stimulation
Categories
Funding
- NHLBI NIH HHS [HL36611] Funding Source: Medline
- NIAID NIH HHS [AI22159] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL036611, R55HL036611] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI022159, R01AI022159] Funding Source: NIH RePORTER
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Toxic shock syndrome (TSS) is an acute onset illness characterized by fever, rash formation, and hypotension that can lead to multiple organ failure and lethal shock, as well as desquamation in patients that recover. The disease is caused by bacterial superantigens (SAGs) secreted from Staphylococcus aureus and group A streptococci. SAGs bypass normal antigen presentation by binding to class II major histocompatibility complex molecules on antigen-presenting cells and to specific variable regions on the beta -chain of the T-cell antigen receptor. Through this interaction, SAGs activate T cells at orders of magnitude above antigen-specific activation, resulting in massive cytokine release that is believed to be responsible for the most severe features of TSS. This review focuses on clinical and epidemiological aspects of TSS, as well as important developments in the genetics, biochemistry, immunology, and structural biology of SAGs. From the evolutionary relationships between these important toxins, we propose that there are five distinct groups of SAGs.
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