ArticleImmunology2014
Defective antiviral CD8 T-cell response and viral clearance in the absence of c-Jun N-terminal kinases.
Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 7 citations in OpenAlex.
- A novel case of autosomal recessive CARD11 loss-of-function underlying impaired antiviral immunity and a review of literature.Clinical & translational immunology · 2026Article
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Chronic mucocutaneous candidiasis and connective tissue disorder in humans with impaired JNK1-dependent responses to IL-17A/F and TGF-β.Science immunology · 2019Article
- Noninvasive Identification of Immune-Related Biomarkers in Hepatocellular Carcinoma.Journal of oncology · 2019Article
- Follistatin-like protein 1 contributes to dendritic cell and T-lymphocyte activation in nasopharyngeal carcinoma patients by altering nuclear factor κb and Jun N-terminal kinase expression.Cell biochemistry and function · 2016Article
- T cell subset profile in healthy Zambian adults at the University Teaching Hospital.The Pan African medical journal · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-Jun N-terminal kinase (JNK) signalling pathway appears to act as a critical intermediate in the regulation of lymphocyte activation and proliferation. The majority of studies on the importance of JNK are focused on its role in T helper responses, with very few reports addressing the mechanisms of JNK in governing CD8 T-cell-mediated immunity. By using a well-defined mousepox model, we demonstrate that JNK is involved in CD8(+) T-cell-mediated antiviral responses. Deficiency of either JNK1 or JNK2 impaired viral clearance, subsequently resulting in an increased susceptibility to ectromelia virus in resistant mice. The impairment of CD8 responses in JNK-deficient mice was not directly due to an inhibition of effector T-cell expansion, as both JNK1 and JNK2 had limited effect on the activation-induced cell death of CD8(+) T cells, and only JNK2-deficient mice exhibited a significant change in CD8(+) T-cell proliferation after acute ectromelia virus infection. However, optimal activation of CD8(+) T cells and their effector functions require signals from both JNK1 and JNK2. Our results suggest that the JNK pathway acts as a critical intermediate in antiviral immunity through regulation of the activation and effector function of CD8(+) T cells rather than by altering their expansion.
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.