ArticleGenes and immunity2016
GWAS analysis implicates NF-κB-mediated induction of inflammatory T cells in multiple sclerosis.
Article in Genes and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 80 citations in OpenAlex.
- Loss of proton-sensing TDAG8 increases tumor progression in mouse models of colon cancer.Molecular oncology · 2026Article
- Article
- Microbiota-Derived SCFAs in Multiple Sclerosis: From Immune Priming to Neurodegeneration.Molecular neurobiology · 2025Review
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- Transcription factors in the development and treatment of immune disorders.Transcription · 2025Review
- Review
- Role of pH-sensing receptors in colitis.Pflugers Archiv : European journal of physiology · 2024Review
- The role of the "gut microbiota-mitochondria" crosstalk in the pathogenesis of multiple sclerosis.Frontiers in microbiology · 2024Review
- OGR1 (GPR68) and TDAG8 (GPR65) Have Antagonistic Effects in Models of Colonic Inflammation.International journal of molecular sciences · 2023Article
- Shared Molecular Signatures Across Zika Virus Infection and Multiple Sclerosis Highlight AP-1 Transcription Factor as a Potential Player in Post-ZIKV MS-Like Phenotypes.Molecular neurobiology · 2023Article
- Review
- Novel NF-κB reporter mouse for the non-invasive monitoring of inflammatory diseases.Scientific reports · 2023Article
- c-Rel-dependent monocytes are potent immune suppressor cells in cancer.Journal of leukocyte biology · 2022Article
- Review
- GPR65 (TDAG8) inhibits intestinal inflammation and colitis-associated colorectal cancer development in experimental mouse models.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Curdlan, a Microbial β-Glucan, Has Contrasting Effects on Autoimmune and Viral Models of Multiple Sclerosis.Frontiers in cellular and infection microbiology · 2022Article
- Prediction of combination therapies based on topological modeling of the immune signaling network in multiple sclerosis.Genome medicine · 2021Article
- Review
- A catalog of GWAS fine-mapping efforts in autoimmune disease.American journal of human genetics · 2021Review
- The contribution of thymic tolerance to central nervous system autoimmunity.Seminars in immunopathology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
To identify genes and biologically relevant pathways associated with risk to develop multiple sclerosis (MS), the Genome-Wide Association Studies noise reduction method (GWAS-NR) was applied to MS genotyping data. Regions of association were defined based on the significance of linkage disequilibrium blocks. Candidate genes were cross-referenced based on a review of current literature, with attention to molecular function and directly interacting proteins. Supplementary annotations and pathway enrichment scores were generated using The Database for Annotation, Visualization and Integrated Discovery. The candidate set of 220 MS susceptibility genes prioritized by GWAS-NR was highly enriched with genes involved in biological pathways related to positive regulation of cell, lymphocyte and leukocyte activation (P=6.1E-15, 1.2E-14 and 5.0E-14, respectively). Novel gene candidates include key regulators of NF-κB signaling and CD4+ T helper type 1 (Th1) and T helper type 17 (Th17) lineages. A large subset of MS candidate genes prioritized by GWAS-NR were found to interact in a tractable pathway regulating the NF-κB-mediated induction and infiltration of pro-inflammatory Th1/Th17 T-cell lineages, and maintenance of immune tolerance by T-regulatory cells. This mechanism provides a biological context that potentially links clinical observations in MS to the underlying genetic landscape that may confer susceptibility.
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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.