To determine the molecular mechanisms of T cell stimulation by staphylococcal enterotoxin A (SEA), we examined the expression of T cell receptor (TcR) Vβ on the T cells from four strains of mice stimulated in vitro with SEA, using flow cytometric analysis for the number of T cells bearing Vβ3, Vβ6, Vβ8, Vβ11 and RNA blotting analysis for the amount of transcripts of Vβ1, Vβ5 and Vβ12. The number of T cell blasts bearing Vβ1, Vβ3, Vβ1 or Vβ12 were increased in the T cell blasts proliferating in vitro in response to SEA in C57BL/6 mice. In AKR/J mice, which contain few Vβ11‐ or Vβ12‐bearing T cells due to a tolerance to the self‐MHC class II IE‐antigens, T cells bearing Vβ1 or Vβ3 responded to SEA. SEA enriched only Vβ1‐bearing T cells in BALB/c mice carrying Mls‐2a which lack Mls‐1a‐reactive Vβ3‐bearing T cells as well as Vβ11‐ and Vβ12‐bearing T cells. In spite of the presence of Vβ1‐bearing T cells, C3H/He T cells exhibited a very low responsiveness to SEA. T cell repertoires skewed by clonal deletion of self‐reactive T cells may in part account for the different sensitivity to SEA among the different strains. A tolerance to SEA can be established in C57BL/6 mice which have been primed i.v. with SEA and treated i.p. with 200 mg/kg of cyclophosphamide 2 days later. All mature T cells bearing Vβ3 or Vβ11 were virtually abolished in the periphery of tolerant mice. These results suggest that most T cells reactive to SEA bear Vβ1, Vβ3, Vβ11 or Vβ12 and that clonal deletion of mature T cells reactive to SEA may account for the cellular mechanisms for cyclophosphamide‐induced tolerance to SEA.
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