GSBS Student Publications

Title

Defective T cell differentiation in the absence of Jnk1

GSBS Program

Biochemistry & Molecular Pharmacology

Publication Date

1998-12-16

UMMS Affiliation

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

Document Type

Article

Disciplines

Life Sciences | Medicine and Health Sciences

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.

Source

Science. 1998 Dec 11;282(5396):2092-5.

Journal/Book/Conference Title

Science (New York, N.Y.)

Related Resources

Link to article in PubMed

PubMed ID

9851932

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