Defective T cell differentiation in the absence of Jnk1
Biochemistry & Molecular Pharmacology
Graduate School of Biomedical Sciences; Howard Hughes Medical Institute, Program in Molecular Medicine
Medical Subject Headings
Animals; Apoptosis; Calcium-Calmodulin-Dependent Protein Kinases; Cell Differentiation; Cell Division; DNA-Binding Proteins; Female; Gene Targeting; Hemocyanin; Interferon Type II; Interleukins; JNK Mitogen-Activated Protein Kinases; *Lymphocyte Activation; Male; Mice; Mice, Knockout; *Mitogen-Activated Protein Kinases; NFATC Transcription Factors; *Nuclear Proteins; Signal Transduction; T-Lymphocytes, Helper-Inducer; Th1 Cells; Th2 Cells; Transcription Factors
Life Sciences | Medicine and Health Sciences
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.
Rights and Permissions
Citation: Science. 1998 Dec 11;282(5396):2092-5.
Science (New York, N.Y.)
Dong, Chen; Yang, Derek D.; Wysk, Mark Allen; Whitmarsh, Alan J.; Davis, Roger J.; and Flavell, Richard A., "Defective T cell differentiation in the absence of Jnk1" (1998). GSBS Student Publications. 321.