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JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development

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JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development. / Sabapathy, K; Hu, Y; Kallunki, T; Schreiber, M; David, J P; Jochum, W; Wagner, E F; Karin, M.

In: CURR BIOL, Vol. 9, No. 3, 11.02.1999, p. 116-25.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Sabapathy, K, Hu, Y, Kallunki, T, Schreiber, M, David, JP, Jochum, W, Wagner, EF & Karin, M 1999, 'JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development', CURR BIOL, vol. 9, no. 3, pp. 116-25.

APA

Sabapathy, K., Hu, Y., Kallunki, T., Schreiber, M., David, J. P., Jochum, W., Wagner, E. F., & Karin, M. (1999). JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development. CURR BIOL, 9(3), 116-25.

Vancouver

Sabapathy K, Hu Y, Kallunki T, Schreiber M, David JP, Jochum W et al. JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development. CURR BIOL. 1999 Feb 11;9(3):116-25.

Bibtex

@article{3b2f410cff23472a87e3e7d309f452df,
title = "JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development",
abstract = "BACKGROUND: The Jun N-terminal kinase (JNK) signaling pathway has been implicated in cell proliferation and apoptosis, but its function seems to depend on the cell type and inducing signal. In T cells, JNK has been implicated in both antigen-induced activation and apoptosis.RESULTS: We generated mice lacking the JNK2 isozymes. The mutant mice were healthy and fertile but defective in peripheral T-cell activation induced by antibody to the CD3 component of the T-cell receptor (TCR) complex - proliferation and production of interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) were reduced. The proliferation defect was restored by exogenous IL-2. B-cell activation was normal in the absence of JNK2. Activation-induced peripheral T-cell apoptosis was comparable between mutant and wild-type mice, but immature (CD4(+) CD8(+)) thymocytes lacking JNK2 were resistant to apoptosis induced by administration of anti-CD3 antibody in vivo. The lack of JNK2 also resulted in partial resistance of thymocytes to anti-CD3 antibody in vitro, but had little or no effect on apoptosis induced by anti-Fas antibody, dexamethasone or ultraviolet-C (UVC) radiation.CONCLUSIONS: JNK2 is essential for efficient activation of peripheral T cells but not B cells. Peripheral T-cell activation is probably required indirectly for induction of thymocyte apoptosis resulting from administration of anti-CD3 antibody in vivo. JNK2 functions in a cell-type-specific and stimulus-dependent manner, being required for apoptosis of immature thymocytes induced by anti-CD3 antibody but not for apoptosis induced by anti-Fas antibody, UVC or dexamethasone. JNK2 is not required for activation-induced cell death of mature T cells.",
keywords = "Animals, Antibodies, Monoclonal, Antigens, CD95, Apoptosis, B-Lymphocytes, Dexamethasone, Drug Resistance, Gene Targeting, Isoenzymes, Lymphocyte Activation, Mice, Mice, Knockout, Mitogen-Activated Protein Kinase 9, Mitogen-Activated Protein Kinases, Muromonab-CD3, Protein Kinases, RNA Splicing, T-Lymphocytes, Ultraviolet Rays",
author = "K Sabapathy and Y Hu and T Kallunki and M Schreiber and David, {J P} and W Jochum and Wagner, {E F} and M Karin",
year = "1999",
month = feb,
day = "11",
language = "English",
volume = "9",
pages = "116--25",
journal = "CURR BIOL",
issn = "0960-9822",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development

AU - Sabapathy, K

AU - Hu, Y

AU - Kallunki, T

AU - Schreiber, M

AU - David, J P

AU - Jochum, W

AU - Wagner, E F

AU - Karin, M

PY - 1999/2/11

Y1 - 1999/2/11

N2 - BACKGROUND: The Jun N-terminal kinase (JNK) signaling pathway has been implicated in cell proliferation and apoptosis, but its function seems to depend on the cell type and inducing signal. In T cells, JNK has been implicated in both antigen-induced activation and apoptosis.RESULTS: We generated mice lacking the JNK2 isozymes. The mutant mice were healthy and fertile but defective in peripheral T-cell activation induced by antibody to the CD3 component of the T-cell receptor (TCR) complex - proliferation and production of interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) were reduced. The proliferation defect was restored by exogenous IL-2. B-cell activation was normal in the absence of JNK2. Activation-induced peripheral T-cell apoptosis was comparable between mutant and wild-type mice, but immature (CD4(+) CD8(+)) thymocytes lacking JNK2 were resistant to apoptosis induced by administration of anti-CD3 antibody in vivo. The lack of JNK2 also resulted in partial resistance of thymocytes to anti-CD3 antibody in vitro, but had little or no effect on apoptosis induced by anti-Fas antibody, dexamethasone or ultraviolet-C (UVC) radiation.CONCLUSIONS: JNK2 is essential for efficient activation of peripheral T cells but not B cells. Peripheral T-cell activation is probably required indirectly for induction of thymocyte apoptosis resulting from administration of anti-CD3 antibody in vivo. JNK2 functions in a cell-type-specific and stimulus-dependent manner, being required for apoptosis of immature thymocytes induced by anti-CD3 antibody but not for apoptosis induced by anti-Fas antibody, UVC or dexamethasone. JNK2 is not required for activation-induced cell death of mature T cells.

AB - BACKGROUND: The Jun N-terminal kinase (JNK) signaling pathway has been implicated in cell proliferation and apoptosis, but its function seems to depend on the cell type and inducing signal. In T cells, JNK has been implicated in both antigen-induced activation and apoptosis.RESULTS: We generated mice lacking the JNK2 isozymes. The mutant mice were healthy and fertile but defective in peripheral T-cell activation induced by antibody to the CD3 component of the T-cell receptor (TCR) complex - proliferation and production of interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) were reduced. The proliferation defect was restored by exogenous IL-2. B-cell activation was normal in the absence of JNK2. Activation-induced peripheral T-cell apoptosis was comparable between mutant and wild-type mice, but immature (CD4(+) CD8(+)) thymocytes lacking JNK2 were resistant to apoptosis induced by administration of anti-CD3 antibody in vivo. The lack of JNK2 also resulted in partial resistance of thymocytes to anti-CD3 antibody in vitro, but had little or no effect on apoptosis induced by anti-Fas antibody, dexamethasone or ultraviolet-C (UVC) radiation.CONCLUSIONS: JNK2 is essential for efficient activation of peripheral T cells but not B cells. Peripheral T-cell activation is probably required indirectly for induction of thymocyte apoptosis resulting from administration of anti-CD3 antibody in vivo. JNK2 functions in a cell-type-specific and stimulus-dependent manner, being required for apoptosis of immature thymocytes induced by anti-CD3 antibody but not for apoptosis induced by anti-Fas antibody, UVC or dexamethasone. JNK2 is not required for activation-induced cell death of mature T cells.

KW - Animals

KW - Antibodies, Monoclonal

KW - Antigens, CD95

KW - Apoptosis

KW - B-Lymphocytes

KW - Dexamethasone

KW - Drug Resistance

KW - Gene Targeting

KW - Isoenzymes

KW - Lymphocyte Activation

KW - Mice

KW - Mice, Knockout

KW - Mitogen-Activated Protein Kinase 9

KW - Mitogen-Activated Protein Kinases

KW - Muromonab-CD3

KW - Protein Kinases

KW - RNA Splicing

KW - T-Lymphocytes

KW - Ultraviolet Rays

M3 - SCORING: Journal article

C2 - 10021384

VL - 9

SP - 116

EP - 125

JO - CURR BIOL

JF - CURR BIOL

SN - 0960-9822

IS - 3

ER -