Defective T cell differentiation in the absence of Jnk1

C Dong; D D Yang; M Wysk; A J Whitmarsh; R J Davis; R A Flavell

Defective T cell differentiation in the absence of Jnk1

C Dong, D D Yang, M Wysk, A J Whitmarsh, R J Davis, R A Flavell

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	2092-5
Number of pages	4
Journal	Science
Volume	282
Issue number	5396
Publication status	Published - 11 Dec 1998

Keywords

Animals
Apoptosis
Calcium-Calmodulin-Dependent Protein Kinases
Cell Differentiation
Cell Division
DNA-Binding Proteins
Female
Gene Targeting
Hemocyanin
Interferon-gamma
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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Cite this

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title = "Defective T cell differentiation in the absence of Jnk1",

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.",

keywords = "Animals, Apoptosis, Calcium-Calmodulin-Dependent Protein Kinases, Cell Differentiation, Cell Division, DNA-Binding Proteins, Female, Gene Targeting, Hemocyanin, Interferon-gamma, 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",

author = "C Dong and Yang, {D D} and M Wysk and Whitmarsh, {A J} and Davis, {R J} and Flavell, {R A}",

year = "1998",

month = dec,

day = "11",

language = "English",

volume = "282",

pages = "2092--5",

journal = "Science",

issn = "0036-8075",

publisher = "American Association for the Advancement of Science (A A A S)",

number = "5396",

}

TY - JOUR

T1 - Defective T cell differentiation in the absence of Jnk1

AU - Dong, C

AU - Yang, D D

AU - Wysk, M

AU - Whitmarsh, A J

AU - Davis, R J

AU - Flavell, R A

PY - 1998/12/11

Y1 - 1998/12/11

N2 - 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.

AB - 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.

KW - Animals

KW - Apoptosis

KW - Calcium-Calmodulin-Dependent Protein Kinases

KW - Cell Differentiation

KW - Cell Division

KW - DNA-Binding Proteins

KW - Female

KW - Gene Targeting

KW - Hemocyanin

KW - Interferon-gamma

KW - Interleukins

KW - JNK Mitogen-Activated Protein Kinases

KW - Lymphocyte Activation

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Mitogen-Activated Protein Kinases

KW - NFATC Transcription Factors

KW - Nuclear Proteins

KW - Signal Transduction

KW - T-Lymphocytes, Helper-Inducer

KW - Th1 Cells

KW - Th2 Cells

KW - Transcription Factors

M3 - Article

C2 - 9851932

SN - 0036-8075

VL - 282

SP - 2092

EP - 2095

JO - Science

JF - Science

IS - 5396

ER -

Defective T cell differentiation in the absence of Jnk1

Abstract

Keywords

UN SDGs

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