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Jun N-terminal kinase 2 modulates thymocyte apoptosis and T cell activation through c-Jun and nuclear factor of

A Behrens1, K Sabapathy, I Graef

  • 1Research Institute of Molecular Pathology, Dr. Bohr-Gasse 7, A-1030 Vienna, Austria.

Proceedings of the National Academy of Sciences of the United States of America
|February 15, 2001
PubMed

Insights

Jun N-terminal kinases (JNKs) are crucial for thymocyte apoptosis but not T cell proliferation. JNK signaling targets both c-Jun and NF-AT, influencing distinct lymphocyte functions.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Signaling

Background:

  • Jun N-terminal kinases (JNKs) play roles in T cell development and function.
  • Understanding JNK signaling pathways is vital for T cell biology.

Purpose of the Study:

  • To investigate the molecular targets of JNK signaling in lymphoid cells.
  • To elucidate the role of c-Jun phosphorylation in JNK-mediated T cell responses.

Main Methods:

  • Utilized homologous recombination to create mice with non-phosphorylatable c-Jun (junAA mice).
  • Analyzed c-Jun phosphorylation, thymocyte apoptosis, and T cell proliferation/differentiation in wild-type and junAA mice.
  • Assessed NF-AT DNA-binding activity and NF-AT-dependent transcription in JNK-deficient T cells and Jurkat cells.

Main Results:

  • c-Jun phosphorylation by JNK is essential for thymocyte apoptosis induced by T cell receptor or TNF-alpha, but not for T cell proliferation or differentiation.
  • JNK2 deficiency in T cells led to reduced NF-AT DNA-binding activity.
  • JNK2 overexpression enhanced NF-AT-dependent transcription in Jurkat T cells.

Conclusions:

  • JNK signaling differentially regulates thymocyte apoptosis and T cell proliferation via distinct effectors, c-Jun and NF-AT.
  • JNK2 has substrates beyond c-Jun that are critical for lymphocyte function, including NF-AT activity.

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