ArticleCells2019
IL-6, IL-12, and IL-23 STAT-Pathway Genetic Risk and Responsiveness of Lymphocytes in Patients with Multiple Sclerosis.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- Memory T cell rapid recall is driven by memory-specific AP-1 recruitment determined by epigenome and co-factor interactions.bioRxiv : the preprint server for biology · 2026Article
- Impact of dermatology targeted immunotherapies on autoimmune thyroid diseases: cytokine-network crosstalk and thyroid safety.Frontiers in immunology · 2026Review
- Breaking the Cycle: Can Vitamin D Bridge the Gap Between Gut Microbiota and Immune Dynamics in Multiple Sclerosis?International journal of molecular sciences · 2025Review
- Identification of biomarkers related to propionate metabolism in schizophrenia.Frontiers in psychiatry · 2025Article
- Bushen Zhuyun Decoction Enhances Endometrial Receptivity via the IL-6/STAT3 Signaling Pathway in Rats.Combinatorial chemistry & high throughput screening · 2025Article
- Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications.International journal of molecular sciences · 2023Review
- The presence, severity, and onset of preeclampsia is associated with maternal interleukin-23 level: A case-control study.International journal of reproductive biomedicine · 2023Article
- A retrospective study of myelin oligodendrocyte glycoprotein antibody-associated disease from a clinical laboratory perspective.Frontiers in neurology · 2023Article
- mbDenoise: microbiome data denoising using zero-inflated probabilistic principal components analysis.Genome biology · 2022Article
- JAK-STAT Pathway Inhibition and their Implications in COVID-19 Therapy.Postgraduate medicine · 2021Review
- COVID-19: Characteristics and Therapeutics.Cells · 2021Review
- Cytokines that Modulate the Differentiation of Th17 Cells in Autoimmune Uveitis.Journal of immunology research · 2021Review
- Cytokines and Transgenic Matrix in Autoimmune Diseases: Similarities and Differences.Biomedicines · 2020Review
- Epistatic evidence for gender-dependant slow neurotransmission signalling in substance use disorders: PPP1R12B versus PPP1R1B.EBioMedicine · 2020Article
- Immunology of IL-12: An update on functional activities and implications for disease.EXCLI journal · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an immune-mediated demyelinating disease characterized by central nervous system (CNS) lymphocyte infiltration, abundant production of pro-inflammatory cytokines, and inappropriate activation of Th1 and Th17 cells, B cells, and innate immune cells. The etiology of MS is complex, and genetic factors contribute to disease susceptibility. Genome-wide association studies (GWAS) have revealed numerous MS-risk alleles in the IL-6/STAT3, IL-12/STAT4, and IL-23/STAT3-pathways implicated in the differentiation of Th1 and Th17 cells. In this study, we investigated the signaling properties of these pathways in T, B, and NK cells from patients with relapsing-remitting MS (RRMS) and healthy controls, and assessed the genetic contribution to the activity of the pathways. This revealed a great variability in the level of STAT-pathway molecules and STAT activation between the cell types investigated. We also found a strong donor variation in IL-6, IL-12, and IL-23 responsiveness of primed CD4+ T cells. This variation could not be explained by a single MS-risk variant in a pathway component, or by an accumulation of multiple STAT-pathway MS-risk SNPs. The data of this study suggests that other factors in cohesion with the genetic background contribute to the responsiveness of the IL-6/STAT3, IL-12/STAT4, and IL-23/STAT3-pathways.
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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.