Defective T cell differentiation in the absence of Jnk1.
basic_science · Level V
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- Record sourced from PubMed, PMID 9851932.
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Abstract
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.
Medical subject headings
- Calcium-Calmodulin-Dependent Protein Kinases
- Lymphocyte Activation
- Mitogen-Activated Protein Kinases
- Nuclear Proteins
- T-Lymphocytes, Helper-Inducer