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To determine the molecular mechanisms of T cell stimulation by staphylococcal enterotoxin A (SEA), we examined the expression of T cell receptor (TcR) V beta 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 V beta 3, V beta 6, V beta 8, V beta 11 and RNA blotting analysis for the amount of transcripts of V beta 1, V beta 5 and V beta 12. The number of T cell blasts bearing V beta 1, V beta 3, V beta 1 or V beta 12 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 V beta 11- or V beta 12-bearing T cells due to a tolerance to the self-MHC class II IE-antigens, T cells bearing V beta 1 or V beta 3 responded to SEA. SEA enriched only V beta 1-bearing T cells in BALB/c mice carrying Mls-2a which lack Mls-1a-reactive V beta 3-bearing T cells as well as V beta 11- and V beta 12-bearing T cells. In spite of the presence of V beta 1-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 V beta 3 or V beta 11 were virtually abolished in the periphery of tolerant mice. These results suggest that most T cells reactive to SEA bear V beta 1, V beta 3, V beta 11 or V beta 12 and that clonal deletion of mature T cells reactive to SEA may account for the cellular mechanisms for cyclophosphamide-induced tolerance to SEA.
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
May 1989,
Science (New York, N.Y.),
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
March 1996,
Scandinavian journal of immunology,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
August 1990,
Nature,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
August 1991,
Immunology letters,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
December 1990,
Japanese journal of medical science & biology,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
January 1989,
Cell,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
October 1990,
The Journal of experimental medicine,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
August 1993,
Immunology,
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
April 2003,
Journal of immunology (Baltimore, Md. : 1950),
H Takimoto, and
Y Yoshikai, and
K Kishihara, and
G Matsuzaki, and
H Kuga, and
T Otani, and
K Nomoto
June 1990,
Journal of immunology (Baltimore, Md. : 1950),
