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

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

Research output: Contribution to journalArticlepeer-review

287 Scopus citations


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 (US)
Pages (from-to)91-94
Number of pages4
Issue number6782
StatePublished - May 4 2000

All Science Journal Classification (ASJC) codes

  • General


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