ArticleImmunology2015
The p38 mitogen-activated protein kinase cascade modulates T helper type 17 differentiation and functionality in multiple sclerosis.
Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.Retrovirology · 2015Pooled it
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- Inflammation mechanism and anti-inflammatory therapy of dry eye.Frontiers in medicine · 2024Review
- Biapenem, a Carbapenem Antibiotic, Elicits Mycobacteria Specific Immune Responses and Reduces the Recurrence of Tuberculosis.Microbiology spectrum · 2023Article
- Article
- The therapeutic potential of triptolide and celastrol in neurological diseases.Frontiers in pharmacology · 2022Review
- Understanding Abnormal c-JNK/p38MAPK Signaling Overactivation Involved in the Progression of Multiple Sclerosis: Possible Therapeutic Targets and Impact on Neurodegenerative Diseases.Neurotoxicity research · 2021Review
- Superoxide Dismutase 3 Controls the Activation and Differentiation of CD4Frontiers in immunology · 2021Article
- Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences.Biomedicines · 2020Review
- The sex-specific role of p38 MAP kinase in CNS autoimmunity is regulated by estrogen receptor alpha.Journal of neuroimmunology · 2020Article
- Celastrol suppresses experimental autoimmune encephalomyelitis via MAPK/SGK1-regulated mediators of autoimmune pathology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Phosphatase PP2A is essential for TProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Aberrant STAT phosphorylation signaling in peripheral blood mononuclear cells from multiple sclerosis patients.Journal of neuroinflammation · 2018Article
- Identifying characteristic miRNAs-genes and risk pathways of multiple sclerosis based on bioinformatics analysis.Oncotarget · 2018Article
- Unique properties of TCR-activated p38 are necessary for NFAT-dependent T-cell activation.PLoS biology · 2018Article
- Leucine-rich alpha 2 glycoprotein promotes Th17 differentiation and collagen-induced arthritis in mice through enhancement of TGF-β-Smad2 signaling in naïve helper T cells.Arthritis research & therapy · 2017Article
- Inhibition of lysophosphatidic acid receptor ameliorates Sjögren's syndrome in NOD mice.Oncotarget · 2017Article
- Prioritizing biological pathways by recognizing context in time-series gene expression data.BMC bioinformatics · 2016Article
- Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
The p38 mitogen-activated protein kinase cascade is required for the induction of a T helper type 17 (Th17) -mediated autoimmune response, which underlies the development and progression of several autoimmune diseases, such as experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis (MS). However, the contribution of p38 phosphorylation to human Th cell differentiation has not been clarified. Here we demonstrate that the p38 signalling pathway is implicated in the generation of Th17 lymphocytes from human CD4(+) CD27(+) CD45RA(+) naive T cells, both in healthy donors and in patients affected by the relapsing-remitting form of MS. Our data also indicate that p38 activation is essential for interleukin-17 release from central memory lymphocytes and committed Th17 cell clones. Furthermore, CD4(+) T cells isolated from individuals with relapsing-remitting MS display an altered responsiveness of the p38 cascade, resulting in increased p38 phosphorylation upon stimulation. These findings suggest that the p38 signalling pathway, by modulating the Th17 differentiation and response, is involved in the pathogenesis of MS, and open new perspectives for the use of p38 inhibitors in the treatment of Th17-mediated autoimmune diseases.
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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.