JNK is required for effector T-cell function but not for T-cell activation

Cathy Tournier, Chen Dong, Derek D. Yang, Cathy Tournler, Alan J. Whitmarsh, Jie Xu, Roger J. Davis, Richard A. Flavell

    Research output: Contribution to journalArticlepeer-review

    Abstract

    The hallmark of T-cell activation is the production of interleukin 2 (IL-2). c-Jun amino-terminal kinase (JNK), a MAP kinase that phosphorylates c-Jun and other components of the AP-1 group of transcription factors, has been implicated in the activation of IL-2 expression. Previously, we found that T cells from mice deficient in the Jnk1 or Jnk2 gene can be activated and produce IL-2 normally, but are deficient in functional differentiation into Th1 or Th2 subsets. However, studies of mice with compound mutations indicate that JNK1 and JNK2 are redundant during mouse development. Here we use three new mouse models in which peripheral T cells completely lack JNK proteins or signalling, to test whether the JNK signalling pathway is crucial for IL-2 expression and T-cell activation. Unexpectedly, these T cells made more IL-2 and proliferated better than wild-type cells. However, production of effector T-cell cytokines did require JNK. Thus, JNK is necessary for T- cell differentiation but not for naive T-cell activation.
    Original languageEnglish
    Pages (from-to)91-94
    Number of pages3
    JournalNature
    Volume405
    Issue number6782
    DOIs
    Publication statusPublished - 4 May 2000

    Fingerprint

    Dive into the research topics of 'JNK is required for effector T-cell function but not for T-cell activation'. Together they form a unique fingerprint.

    Cite this