ArticleJournal of neuroimmunology2014
RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis.
Article in Journal of neuroimmunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- T-bet Regulates Ion Channels and Transporters and Induces Apoptosis in Intestinal Epithelial Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Adjuvant Injections Altered the Ileal and Fecal Microbiota Differently with Changes in Immunoglobulin Isotypes and Antimycobacterial Antibody Responses.International journal of molecular sciences · 2023Article
- RORγt phosphorylation protects against T cell-mediated inflammation.Cell reports · 2022Article
- Impact of histone modifier-induced protection against autoimmune encephalomyelitis on multiple sclerosis treatment.Frontiers in neurology · 2022Review
- Curcumin β-D-Glucuronide Modulates an Autoimmune Model of Multiple Sclerosis with Altered Gut Microbiota in the Ileum and Feces.Frontiers in cellular and infection microbiology · 2021Article
- Treatment of autoimmune encephalomyelitis with a histone deacetylase inhibitor.Free neuropathology · 2020Article
- Oxysterols in Autoimmunity.International journal of molecular sciences · 2019Review
- Bioinformatics Analyses Determined the Distinct CNS and Peripheral Surrogate Biomarker Candidates Between Two Mouse Models for Progressive Multiple Sclerosis.Frontiers in immunology · 2019Article
- Genistein modulates the expression of Toll-like receptors in experimental autoimmune encephalomyelitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- T-bet, but not Gata3, overexpression is detrimental in a neurotropic viral infection.Scientific reports · 2017Article
- Article
- Three immune-mediated disease models induced by Theiler's virus: Multiple sclerosis, seizures and myocarditis.Clinical & experimental neuroimmunology · 2016Article
- Altered Expression of Specific Transcription Factors of Th17 (RORγt, RORα) and Treg Lymphocytes (FOXP3) by Peripheral Blood Mononuclear Cells from Patients with Multiple Sclerosis.Journal of molecular neuroscience : MN · 2016Article
- Reciprocal regulation of RORγt acetylation and function by p300 and HDAC1.Scientific reports · 2015Article
- The Dynamics of Treg/Th17 and the Imbalance of Treg/Th17 in Clonorchis sinensis-Infected Mice.PloS one · 2015Article
- Different Expressions of Specific Transcription Factors of Th1 (Basic and clinical neuroscienceArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.
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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.