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

Chen Dong, Derek D. Yang, Cathy Tournier, Alan J. Whitmarsh, Jie Xu, Roger J. Davis and Richard A. Flavell
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Chen Dong: Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine
Derek D. Yang: Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine
Cathy Tournier: Howard Hughes Medical Institute Program in Molecular Medicine
Alan J. Whitmarsh: Howard Hughes Medical Institute Program in Molecular Medicine
Jie Xu: Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine
Roger J. Davis: Lilly Research Laboratories
Richard A. Flavell: Howard Hughes Medical Institute, Section of Immunobiology, Yale University School of Medicine

Nature, 2000, vol. 405, issue 6782, 91-94

Abstract: 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 factors1,2, has been implicated in the activation of IL-2 expression3,4. 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 subsets5,6. However, studies of mice with compound mutations indicate that JNK1 and JNK2 are redundant during mouse development7. 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.

Date: 2000
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DOI: 10.1038/35011091

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