T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells

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Standard

T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells. / Claesson, M H; Dissing, S; Tscherning, T; Geisler, C.

In: Immunology, Vol. 78, No. 3, 1993, p. 444-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Claesson, MH, Dissing, S, Tscherning, T & Geisler, C 1993, 'T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells', Immunology, vol. 78, no. 3, pp. 444-8.

APA

Claesson, M. H., Dissing, S., Tscherning, T., & Geisler, C. (1993). T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells. Immunology, 78(3), 444-8.

Vancouver

Claesson MH, Dissing S, Tscherning T, Geisler C. T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells. Immunology. 1993;78(3):444-8.

Author

Claesson, M H ; Dissing, S ; Tscherning, T ; Geisler, C. / T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells. In: Immunology. 1993 ; Vol. 78, No. 3. pp. 444-8.

Bibtex

@article{2339f210b0a711ddb538000ea68e967b,
title = "T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells",
abstract = "We have studied activation-induced changes in intracellular calcium [Ca2+]i, interleukin-2 (IL-2) secretion, and clonal abortion of the human leukaemic T-cell line Jurkat and three T-cell receptor (TcR)/CD3 receptor negative clones deficient for the TcR alpha, TcR beta and CD3 gamma chains respectively, as well as three transfectant clones reconstituted with the appropriate TcR/CD3 cDNA. For activation, the cells were exposed to anti-TcR/CD3, anti-CD2 and anti-major histocompatibility complex (anti-MHC) class I monoclonal antibodies (mAb) respectively. Cellular activation by these mAb leading to an increased IL-2 secretion was preceded by a rise in [Ca2+]i and was relatively dependent on the expression of the a TcR/CD3 complex. In contrast, anti-MHC class I mAb-induced clonal abortion in Jurkat T cells may occur without previous fluctuations in [Ca2+]i and appeared to be independent of TcR/CD3 expression. The present observation suggest the existence of different secondary messenger systems operating in Jurkat cells following activation via the TcR/CD3, CD2 and the MHC class I pathways, respectively.",
author = "Claesson, {M H} and S Dissing and T Tscherning and C Geisler",
note = "Keywords: Antigens, CD2; Antigens, CD3; Antigens, Differentiation, T-Lymphocyte; Calcium; Cell Line; Histocompatibility Antigens Class I; Humans; Interleukin-2; Leukemia, T-Cell; Lymphocyte Activation; Mutation; Neoplastic Stem Cells; Receptors, Immunologic; T-Lymphocytes; Transfection; Tumor Cells, Cultured",
year = "1993",
language = "English",
volume = "78",
pages = "444--8",
journal = "Immunology",
issn = "0019-2805",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - T-cell activation. V. Anti-major histocompatibility complex class I antibody-induced activation and clonal abortion in Jurkat T-leukaemic cells

AU - Claesson, M H

AU - Dissing, S

AU - Tscherning, T

AU - Geisler, C

N1 - Keywords: Antigens, CD2; Antigens, CD3; Antigens, Differentiation, T-Lymphocyte; Calcium; Cell Line; Histocompatibility Antigens Class I; Humans; Interleukin-2; Leukemia, T-Cell; Lymphocyte Activation; Mutation; Neoplastic Stem Cells; Receptors, Immunologic; T-Lymphocytes; Transfection; Tumor Cells, Cultured

PY - 1993

Y1 - 1993

N2 - We have studied activation-induced changes in intracellular calcium [Ca2+]i, interleukin-2 (IL-2) secretion, and clonal abortion of the human leukaemic T-cell line Jurkat and three T-cell receptor (TcR)/CD3 receptor negative clones deficient for the TcR alpha, TcR beta and CD3 gamma chains respectively, as well as three transfectant clones reconstituted with the appropriate TcR/CD3 cDNA. For activation, the cells were exposed to anti-TcR/CD3, anti-CD2 and anti-major histocompatibility complex (anti-MHC) class I monoclonal antibodies (mAb) respectively. Cellular activation by these mAb leading to an increased IL-2 secretion was preceded by a rise in [Ca2+]i and was relatively dependent on the expression of the a TcR/CD3 complex. In contrast, anti-MHC class I mAb-induced clonal abortion in Jurkat T cells may occur without previous fluctuations in [Ca2+]i and appeared to be independent of TcR/CD3 expression. The present observation suggest the existence of different secondary messenger systems operating in Jurkat cells following activation via the TcR/CD3, CD2 and the MHC class I pathways, respectively.

AB - We have studied activation-induced changes in intracellular calcium [Ca2+]i, interleukin-2 (IL-2) secretion, and clonal abortion of the human leukaemic T-cell line Jurkat and three T-cell receptor (TcR)/CD3 receptor negative clones deficient for the TcR alpha, TcR beta and CD3 gamma chains respectively, as well as three transfectant clones reconstituted with the appropriate TcR/CD3 cDNA. For activation, the cells were exposed to anti-TcR/CD3, anti-CD2 and anti-major histocompatibility complex (anti-MHC) class I monoclonal antibodies (mAb) respectively. Cellular activation by these mAb leading to an increased IL-2 secretion was preceded by a rise in [Ca2+]i and was relatively dependent on the expression of the a TcR/CD3 complex. In contrast, anti-MHC class I mAb-induced clonal abortion in Jurkat T cells may occur without previous fluctuations in [Ca2+]i and appeared to be independent of TcR/CD3 expression. The present observation suggest the existence of different secondary messenger systems operating in Jurkat cells following activation via the TcR/CD3, CD2 and the MHC class I pathways, respectively.

M3 - Journal article

C2 - 8097490

VL - 78

SP - 444

EP - 448

JO - Immunology

JF - Immunology

SN - 0019-2805

IS - 3

ER -

ID: 8546057