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About the Authors:
Gabriela A. Ferreyra
Affiliation: Functional Genomics and Proteomics Facility, Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland, United States of America
Jason M. Elinoff
Affiliation: Functional Genomics and Proteomics Facility, Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland, United States of America
Cumhur Y. Demirkale
Affiliation: Mathematical and Statistical Computing Laboratory, Center for Information Technology, National Institutes of Health, Bethesda, Maryland, United States of America
Matthew F. Starost
Affiliation: Division of Veterinary Resources, Office of Research Services, National Institutes of Health, Bethesda, Maryland, United States of America
Marilyn Buckley
Affiliation: Integrated Toxicology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, United States of America
Peter J. Munson
Affiliation: Mathematical and Statistical Computing Laboratory, Center for Information Technology, National Institutes of Health, Bethesda, Maryland, United States of America
Teresa Krakauer
* E-mail: [email protected] (TK); [email protected] (RLD)
Affiliation: Integrated Toxicology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, United States of America
Robert L. Danner
* E-mail: [email protected] (TK); [email protected] (RLD)
Affiliation: Functional Genomics and Proteomics Facility, Critical Care Medicine Department, Clinical Research Center, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Toxic shock [1], [2] overlaps clinically with septic shock [3], [4] and host cytokine release contributes to the pathogenesis of both syndromes. However, unlike septic shock, toxic shock syndrome can occur in the absence of overt infection [1] and the underlying mechanism of immune activation is unique [5], [6], [7]. Toxic shock syndrome toxin 1 (TSST-1) and other exotoxins associated with toxic shock such as staphylococcal enterotoxin B (SEB) are commonly called superantigens. These bacterial toxins bind to the variable region of the T-cell receptor (TCR) beta chain (Vβ) and major histocompatibility complex (MHC) class II molecules on antigen presenting cells (APCs) [5], [8], [9], [10], [11], [12], [13]. The bridging of both cells by superantigen, along with the participation of co-receptors, CD28 on T-cells and CD80 on APCs, leads to massive polyclonal T-cell activation that can result in cytokine storm, shock, organ injury, and death [6], [7], [14]. As humans are extremely sensitive to SEB, especially by inhalation, this superantigen is considered a potential bioterrorism threat [15].
Currently, there are...