ArticleThe Journal of experimental medicine2002
c-Jun NH(2)-terminal kinase (JNK)1 and JNK2 have distinct roles in CD8(+) T cell activation.
Article in The Journal of experimental medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
61 citing papers in PubMed, 146 citations in OpenAlex.
- Modulating AP-1 enables CAR T cells to establish an intratumoral stemlike reservoir and overcomes resistance to PD-1 blockade.Science immunology · 2026Article
- JNK knockdown enhances CAR-T cell cytotoxicity through elevated NFATc1-dependent transcription in preclinical ovarian cancer models.Journal for immunotherapy of cancer · 2025Article
- Role of C-Jun N-Terminal Kinases on a Stressed Epithelium: Time for Testing Isoform Specificity.Biology · 2025Review
- QRICH1 mediates an intracellular checkpoint for CD8Science immunology · 2025Article
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- The POSH scaffold protein is essential for signal coordination leading to CD8 T cell differentiation and survival.Frontiers in immunology · 2025Article
- PCSK9 in T-cell function and the immune response.Biomarker research · 2024Review
- Comparative analysis of methods to reduce activation signature gene expression in PBMCs.Scientific reports · 2023Article
- Single-cell atlas of the aging mouse colon.iScience · 2022Article
- Network Pharmacology and Molecular Docking Analysis on Molecular Mechanism of Qingzi Zhitong Decoction in the Treatment of Ulcerative Colitis.Frontiers in pharmacology · 2022Article
- T cell receptor (TCR) signaling in health and disease.Signal transduction and targeted therapy · 2021Review
- Stress kinases in the development of liver steatosis and hepatocellular carcinoma.Molecular metabolism · 2021Review
- JNK in Tumor Microenvironment: Present Findings and Challenges in Clinical Translation.Cancers · 2021Review
- JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021Review
- Identification of Breast Cancer Immune Subtypes by Analyzing Bulk Tumor and Single Cell Transcriptomes.Frontiers in cell and developmental biology · 2021Article
- Review
- Activation of c-Jun N-Terminal Kinase, a Potential Therapeutic Target in Autoimmune Arthritis.Cells · 2020Review
- Rationalized inhibition of mixed lineage kinase 3 and CD70 enhances life span and antitumor efficacy of CD8Journal for immunotherapy of cancer · 2020Article
- Article
- Mixed lineage kinase 3 inhibition induces T cell activation and cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Jun NH(2)-terminal kinase (JNK) signaling pathway is induced by cytokines and stress stimuli and is implicated in cell death and differentiation, but the specific function of this pathway depends on the cell type. Here we examined the role of JNK1 and JNK2 in CD8(+) T cells. Unlike CD4(+) T cells, the absence of JNK2 causes increased interleukin (IL)-2 production and proliferation of CD8(+) T cells. In contrast, JNK1-deficient CD8(+) T cells are unable to undergo antigen-stimulated expansion in vitro, even in the presence of exogenous IL-2. The hypoproliferation of these cells is associated with impaired IL-2 receptor alpha chain (CD25) gene and cell surface expression. The reduced level of nuclear activating protein 1 (AP-1) complexes in activated JNK1-deficient CD8(+) T cells can account for the impaired IL-2 receptor alpha chain gene expression. Thus, JNK1 and JNK2 play different roles during CD8(+) T cell activation and these roles differ from those in CD4(+) T cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.