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
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.
DOI of Published Version
Science. 1998 Dec 11;282(5396):2092-5.
Science (New York, N.Y.)
Dong C, Yang DD, Wysk MA, Whitmarsh AJ, Davis RJ, Flavell RA. (1998). Defective T cell differentiation in the absence of Jnk1. GSBS Student Publications. https://doi.org/10.1126/science.282.5396.2092. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/321