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Research summary · AI summary · not yet reviewedAnimal studyNot reportedPublished in a peer-reviewed journal
Mouse Models of Multiple Sclerosis and Colitis
Deleting REV-ERBβ in mouse models led to increased TH17-mediated pro-inflammatory cytokine expression and worsened symptoms of multiple sclerosis and colitis.
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- #MSResearch
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This plain-English summary was written by AI from a published abstract and may contain errors. It is not medical advice. Read the original study and talk to your MS team before making decisions about treatment.
- Human efficacy
- Not yet tested in people
- Mechanism
- Not reported
- Evidence strength
- Early – laboratory or animal research
- Outcome
- Negative
Results in cells or animals often do not carry over to people with MS.
Why it matters
This research highlights the role of REV-ERBβ in regulating inflammation, which could be important for understanding the mechanisms underlying multiple sclerosis and similar conditions.
What this does not prove
The study is limited to mouse models and does not provide any evidence of clinical efficacy in humans.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Not reported
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-10-15
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Not classified
- Biological target
- REV-ERBβ
- Pathway
- Not reported
- Population
- Mouse models of multiple sclerosis and colitis
- Size of effect
- Not reported
- Secondary endpoints
- Not reported
- MRI endpoints
- Not reported
- Biomarkers
- Not reported
- Safety
- Not reported
Original sources
- Primary evidenceNegative regulation of TH17-mediated inflammation by the nuclear receptor REV-ERBβ. ↗DOI: 10.1016/j.isci.2026.117577
Supporting passages (13)
publication date2026-10-15
interventionOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
comparatorOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
primary endpointOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
findingsOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
findingsOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
biological targetsREV-ERBβ
populationOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
outcomeNegative
limitationsTitle: Negative regulation of TH17-mediated inflammation by the nuclear receptor REV-ERBβ.
peer reviewedPublication types: Journal Article
subjectsOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
human efficacyOur data indicate that deletion of REV-ERBβ enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis.
AI assessment, not yet reviewed by a person · version 1 · Community votes are separate from evidence review.