# Targeting mitochondrial Kv1.3 enables precise autoreactive T cell therapy for multiple sclerosis

**Authors:** Stefano Pluchino, Cory M Willis

PMC · DOI: 10.1038/s44321-025-00306-3 · EMBO Molecular Medicine · 2025-09-29

## TL;DR

A new therapy for multiple sclerosis targets the mitochondrial Kv1.3 channel in harmful T cells to reduce disease effects without broad immune suppression.

## Contribution

The study introduces a novel therapeutic strategy targeting the mitochondrial Kv1.3 channel in autoreactive T cells for multiple sclerosis.

## Key findings

- Targeting mitochondrial Kv1.3 in autoreactive T cells reduces MS-like pathology.
- This approach offers a more selective treatment compared to current broad immunosuppressive therapies.

## Abstract

Multiple sclerosis (MS), a chronic autoimmune disorder, is characterized by the infiltration of autoreactive T cells into the central nervous system (CNS), leading to myelin destruction and neurological deficits. Current therapies often lack specificity, resulting in broad immunosuppression and potential side effects. In this issue of EMBO Molecular Medicine, Angi, Varanita and colleagues (Angi et al, 2025) identify a novel therapeutic strategy in targeting the mitochondrial Kv1.3 channel in autoreactive T cells, offering a more selective approach to mitigate MS-like pathology.

Pluchino and Willis discuss a study by Szabo et al (in this issue of EMBO Mol Med) that reveals a novel therapy to treat multiple sclerosis by targeting the mitochondrial Kv1.3 channel in autoreactive T cells.

## Linked entities

- **Proteins:** KCNA3 (potassium voltage-gated channel subfamily A member 3)
- **Diseases:** multiple sclerosis (MONDO:0005301)

## Full-text entities

- **Genes:** KCNA3 (potassium voltage-gated channel subfamily A member 3) [NCBI Gene 3738] {aka HGK5, HLK3, HPCN3, HUKIII, KV1.3, MK3}
- **Diseases:** multiple sclerosis (MESH:D009103)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12603289/full.md

## References

1 references — full list in the complete paper: https://tomesphere.com/paper/PMC12603289/full.md

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Source: https://tomesphere.com/paper/PMC12603289