IMMUNOLOGY2026™ Conference Recordings For Attendees-Copper Shapes T Cell Metabolism and Epigenetics to Drive Pathogenic Th17 Cell Function in Autoimmunity

Copper Shapes T Cell Metabolism and Epigenetics to Drive Pathogenic Th17 Cell Function in Autoimmunity

Video Transcription

Video Summary

The talk presented research showing that copper transport via CTR1/SLC31A1 is crucial for pathogenic Th17 cells in autoimmunity. Using a targeted screen in an EAE mouse model of multiple sclerosis, the team identified CTR1 as an important hit. T cell–specific knockout of CTR1 lowered intracellular copper and impaired mitochondrial respiration, forcing cells to increase glycolysis.<br /><br />This metabolic shift altered key metabolites linked to epigenetic regulation, causing increased DNA methylation and reduced chromatin accessibility at important Th17 gene regions. As a result, pathogenic Th17 cells failed to express key transcription factors and cytokines such as RORγt, IL-17A, and GM-CSF.<br /><br />The effect was specific to Th17 cells, with Th1 and Treg programs largely intact. In vivo, CTR1-deficient T cells protected mice from EAE, reducing immune infiltration and demyelination in the spinal cord. Overall, the study suggests copper uptake is a critical driver of pathogenic Th17 function and a potential therapeutic target in autoimmunity.

Meta Tag

Date April 16, 2026 10:15 AM - 10:30 AM

Room 153AB

Session Epigenetics and Post-Transcriptional Regulation

Speaker Lucile Noyer

Track Immune Response Regulation: Molecular Mechanisms (IRM)

Year 2026

Keywords

CTR1/SLC31A1

copper transport

Th17 cells

autoimmunity

EAE model

April 16, 2026 10:15 AM - 10:30 AM

153AB

Epigenetics and Post-Transcriptional Regulation

Lucile Noyer

Immune Response Regulation: Molecular Mechanisms (IRM)

2026