| Literature DB >> 2117641 |
Y Choi1, J A Lafferty, J R Clements, J K Todd, E W Gelfand, J Kappler, P Marrack, B L Kotzin.
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.Entities:
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Year: 1990 PMID: 2117641 PMCID: PMC2188536 DOI: 10.1084/jem.172.3.981
Source DB: PubMed Journal: J Exp Med ISSN: 0022-1007 Impact factor: 14.307