# CD4+CD25+ regulatory T cell therapy in neurological autoimmune diseases

**Authors:** Guobin Yuan, Ying Liu, Hongquan Wang, Tingting Yang, Guangzhi Liu

PMC · DOI: 10.7717/peerj.19450 · 2025-06-12

## TL;DR

This paper explores how CD4+CD25+ regulatory T cells could be used as a therapy for autoimmune diseases affecting the nervous system.

## Contribution

The paper reviews recent advancements and challenges in using CD4+CD25+ Tregs for treating neurological autoimmune diseases.

## Key findings

- CD4+CD25+ Tregs are crucial for immune tolerance and disease progression in neurological autoimmunity.
- Various methods for generating and expanding Tregs are being studied for therapeutic use.
- Cellular therapy using Tregs faces challenges in clinical application.

## Abstract

CD4+CD25+ regulatory T cells (Tregs) play a critical role in maintaining immune tolerance. They are essential for the initiation and progression of autoimmune diseases affecting the nervous system. Recently, the correlation between Tregs and neurological autoimmune diseases, as well as their therapeutic potential, has become a central focus of research. Currently, various methods for in vivo or in vitro generation and expansion of CD4+CD25+ Tregs are under investigation; however, their application in cellular therapy is anticipated to face additional challenges. This article primarily delves into the development and function of CD4+CD25+ Tregs, the role of Tregs in neurological autoimmune disease pathology, basic methods for enhancing therapies, and recent advancements and challenges in cellular therapy for neurological autoimmune diseases.

## Full-text entities

- **Genes:** CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, IL2RA (interleukin 2 receptor subunit alpha) [NCBI Gene 3559] {aka CD25, IDDM10, IL2R, IMD41, TCGFR, p55}
- **Diseases:** neurological autoimmune disease (MESH:D020274), autoimmune diseases (MESH:D001327)

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12169171/full.md

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Source: https://tomesphere.com/paper/PMC12169171