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Cited by 453

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Differentiation of CD4+ T Cells to Th1 Cells Requires MAP Kinase JNK2

Open access
Yang, Derek D, Conze, Dietrich, Whitmarsh, Alan J, Barrett, Tamera, Davis, Roger J, Rincón, Mercedes, Flavell, Richard A·1998·Immunity
DOI 10.1016/s1074-7613(00)80640-8
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Abstract

Precursor CD4+ T cells develop into effector Th1 and Th2 cells that play a central role in the immune response. We show that the JNK MAP kinase pathway is induced in Th1 but not in Th2 effector cells upon antigen stimulation. Further, the differentiation of precursor CD4+ T cells into effector Th1 but not Th2 cells is impaired in JNK2-deficient mice. The inability of IL-12 to differentiate JNK2-deficient CD4+ T cells fully into effector Th1 cells is caused by a defect in IFNgamma production during the early stages of differentiation. The addition of exogenous IFNgamma during differentiation restores IL-12-mediated Th1 polarization in the JNK2-deficient mice. The JNK MAP kinase signaling pathway, therefore, plays an important role in the balance of Th1 and Th2 immune responses.

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Metadata

Authors
Yang, D. D., Conze, D., Whitmarsh, A. J., Barrett, T., Davis, R. J., Rincón, M., & Flavell, R. A.
Venue
Immunity
Publisher
Elsevier BV
Published
1998-10
Volume
9
Issue
4
Pages
575-585
ISSN
1074-7613 (ISSN-L)
DOI
10.1016/s1074-7613(00)80640-8
OpenAlex
W2053560001
Cited by
453
References
4
FWCI
12.66
Type
journal article
Language
en
Open access
hybrid

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.