Defective T cell differentiation in the absence of Jnk1

C Dong, D D Yang, M Wysk, A J Whitmarsh, R J Davis, R A Flavell

    Research output: Contribution to journalArticlepeer-review


    The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation.

    Original languageEnglish
    Pages (from-to)2092-5
    Number of pages4
    Issue number5396
    Publication statusPublished - 11 Dec 1998


    • Animals
    • Apoptosis
    • Calcium-Calmodulin-Dependent Protein Kinases
    • Cell Differentiation
    • Cell Division
    • DNA-Binding Proteins
    • Female
    • Gene Targeting
    • Hemocyanin
    • Interferon-gamma
    • Interleukins
    • JNK Mitogen-Activated Protein Kinases
    • Lymphocyte Activation
    • Male
    • Mice
    • Mice, Knockout
    • Mitogen-Activated Protein Kinases
    • NFATC Transcription Factors
    • Nuclear Proteins
    • Signal Transduction
    • T-Lymphocytes, Helper-Inducer
    • Th1 Cells
    • Th2 Cells
    • Transcription Factors


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