Stimulation of all T cells bearing Vβ1, Vβ3, Vβ11 and Vβ12 by staphylococcal enterotoxin A

Hiroaki Takimoto, Yasunobu Yoshikai, Kenji Kishihara, Goro Matsuzaki, Hiroshi Kuga, Tsuyoshi Otani, Kikuo Nomoto

    Research output: Contribution to journalArticle

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    Abstract

    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.

    Original languageEnglish
    Pages (from-to)617-621
    Number of pages5
    JournalEuropean Journal of Immunology
    Volume20
    Issue number3
    DOIs
    Publication statusPublished - Jan 1 1990

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    T-Lymphocytes
    Clonal Deletion
    Staphylococcal enterotoxin A
    Inbred C57BL Mouse
    Inbred AKR Mouse
    T-Cell Antigen Receptor
    Cyclophosphamide
    RNA

    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Immunology

    Cite this

    Takimoto, H., Yoshikai, Y., Kishihara, K., Matsuzaki, G., Kuga, H., Otani, T., & Nomoto, K. (1990). Stimulation of all T cells bearing Vβ1, Vβ3, Vβ11 and Vβ12 by staphylococcal enterotoxin A. European Journal of Immunology, 20(3), 617-621. https://doi.org/10.1002/eji.1830200323

    Stimulation of all T cells bearing Vβ1, Vβ3, Vβ11 and Vβ12 by staphylococcal enterotoxin A. / Takimoto, Hiroaki; Yoshikai, Yasunobu; Kishihara, Kenji; Matsuzaki, Goro; Kuga, Hiroshi; Otani, Tsuyoshi; Nomoto, Kikuo.

    In: European Journal of Immunology, Vol. 20, No. 3, 01.01.1990, p. 617-621.

    Research output: Contribution to journalArticle

    Takimoto, H, Yoshikai, Y, Kishihara, K, Matsuzaki, G, Kuga, H, Otani, T & Nomoto, K 1990, 'Stimulation of all T cells bearing Vβ1, Vβ3, Vβ11 and Vβ12 by staphylococcal enterotoxin A', European Journal of Immunology, vol. 20, no. 3, pp. 617-621. https://doi.org/10.1002/eji.1830200323
    Takimoto, Hiroaki ; Yoshikai, Yasunobu ; Kishihara, Kenji ; Matsuzaki, Goro ; Kuga, Hiroshi ; Otani, Tsuyoshi ; Nomoto, Kikuo. / Stimulation of all T cells bearing Vβ1, Vβ3, Vβ11 and Vβ12 by staphylococcal enterotoxin A. In: European Journal of Immunology. 1990 ; Vol. 20, No. 3. pp. 617-621.
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    abstract = "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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    AU - Kuga, Hiroshi

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    AU - Nomoto, Kikuo

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