Stimulation of all T cells bearing V beta 1, V beta 3, V beta 11 and V beta 12 by staphylococcal enterotoxin A.
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.
Takimoto
H
H
Department of Immunology, Kyushu University, Fukuoka, Japan.
Yoshikai
Y
Y
Kishihara
K
K
Matsuzaki
G
G
Kuga
H
H
Otani
T
T
Nomoto
K
K
D000818:Animals; D015152:Blotting, Northern; D003208:Concanavalin A / Q000494:pharmacology; D003520:Cyclophosphamide / Q000494:pharmacology; D004768:Enterotoxins / Q000276:immunology*; D005434:Flow Cytometry; D015870:Gene Expression; D007165:Immunosuppression Therapy; D008213:Lymphocyte Activation; D051379:Mice; D008815:Mice, Inbred Strains / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000276:immunology*; D016693:Receptors, Antigen, T-Cell, alpha-beta; D013601:T-Lymphocytes / Q000276:immunology*
D004768:Enterotoxins; D012333:RNA, Messenger; D011948:Receptors, Antigen, T-Cell; D016693:Receptors, Antigen, T-Cell, alpha-beta; D003208:Concanavalin A; C026066:enterotoxin A, Staphylococcal; D003520:Cyclophosphamide