GSBS Student Publications


Defective T cell differentiation in the absence of Jnk1

GSBS Program

Biochemistry & Molecular Pharmacology

UMMS Affiliation

Graduate School of Biomedical Sciences; Howard Hughes Medical Institute, Program in Molecular Medicine



Document Type


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.

Related Resources

Link to article in PubMed

Journal Title

Science (New York, N.Y.)

PubMed ID