Abstract
Infection with Staphylococcus aureus and the production of toxic shock syndrome toxin-1 (TSST-1) have been implicated in the pathogenesis of toxic shock syndrome. Previous in vitro studies have demonstrated that TSST-1 is a powerful but selective stimulator of human T cells, and that the majority of activated cells express the TCR V beta 2 gene segment. We therefore studied patients with toxic shock syndrome using a modification of the PCR to determine if expansion of V beta 2+ T cells is a marker of the in vivo disease process. Five of eight patients studied demonstrated markedly elevated levels of circulating V beta 2+ T cells, whereas none showed significantly elevated levels of T cells expressing other V beta gene segments. The results suggest that toxin-mediated T cell activation, which involves a large fraction of the human T cell repertoire, may be critical in the pathogenesis of this disease.
MeSH Terms
Antigens, CD/analysis
Antigens, Differentiation, T-Lymphocyte/analysis
CD4 Antigens/analysis
CD8 Antigens
Humans
Immunoglobulin Variable Region/genetics
Longitudinal Studies
Receptors, Antigen, T-Cell/genetics
Reference Values
Shock, Septic/immunology
Staphylococcal Infections/immunology
T-Lymphocytes/immunology
Chemicals
Antigens, CD
Antigens, Differentiation, T-Lymphocyte
CD4 Antigens
CD8 Antigens
Immunoglobulin Variable Region
Receptors, Antigen, T-Cell
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Choi Y
Howard Hughes Medical Institute, Denver.
Lafferty J A
Clements J R
Todd J K
Gelfand E W
Kappler J
Marrack P
Kotzin B L
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