Deletion of Slc31a1 in CD4 + T cells
Deleting Slc31a1 in CD4 + T cells led to lower copper levels, disrupting mitochondrial respiration and metabolism, which impaired DNA demethylation. This resulted in hypermethylated DNA and changes in chromatin that affected AP-1 transcription factor binding, crucial for pT H 17 cell differentiation. The Slc31a1 deletion also protected mice from CNS inflammation in an MS model.
- Tags
- #MSResearch
- Most relevant to
- —
- Human efficacy
- Not yet assessed
- Mechanism
- Not yet assessed
- Evidence strength
- Not yet assessed
- Outcome
- Not yet assessed
Why it matters
This research highlights the role of copper in regulating T cell metabolism and function, suggesting a link between copper homeostasis and autoimmunity related to T H 17 cells, potentially influencing future therapeutic strategies.
What this does not prove
The study's findings are based on mouse models, limiting direct relevance to human MS and providing no evidence on how copper affects T cell function 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
- 2026-09-28
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Not classified
Original sources
- Primary evidenceCTR1-mediated copper uptake orchestrates metabolic-epigenetic regulation of pathogenic T H 17 cells in autoimmune disease. ↗DOI: 10.64898/2026.09.22.747582
Supporting passages (4)
interventionMoreover, T cell-specific deletion of Slc31a1 protected mice from central nervous system (CNS) inflammation in the experimental autoimmune encephalomyelitis (EAE) model of MS by suppressing clonal expansion of autoreactive CD4 + T cells.
findingsThese findings establish copper as a critical regulator of pT H 17 differentiation and function, revealing a previously unknown molecular link between copper homeostasis, metabolism and epigenetic regulation governing pT H 17-mediated autoimmunity.
publication datePublication date: 2026-09-28
limitationsTitle: CTR1-mediated copper uptake orchestrates metabolic-epigenetic regulation of pathogenic T H 17 cells in autoimmune disease.
AI assessment, not yet reviewed by a person · version 1 · Community votes are separate from evidence review.