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Defective T Cell Differentiation in the Absence of Jnk1
Abstract
The c-Jun NH 2 -terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (T H ) cells into T H 1 and T H 2 effector cells. JNK activity observed in wild-type activated T H cells was severely reduced in T H cells from Jnk1 –/– mice. The Jnk1 –/– T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to T H 2 cells. The enhanced production of T H 2 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 T H cell proliferation, apoptosis, and differentiation.
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Metadata
- Authors
- Dong, C., Yang, D. D., Wysk, M., Whitmarsh, A. J., Davis, R. J., & Flavell, R. A.
- Venue
- Science
- Published
- 1998-12-11
- Volume
- 282
- Issue
- 5396
- Pages
- 2092-2095
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2086402424
- Cited by
- 584
- References
- 2
- FWCI
- 16.36
- Type
- journal article
- Language
- en
- Open access
- closed
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