# Metabolic checkpoints in the regulation of Th17 cells: implications for uveitis pathogenesis and therapy

## TL;DR

This review explores how metabolic checkpoints in Th17 cells affect uveitis and suggests potential therapeutic strategies based on these findings.

## Contribution

The paper highlights recent advances in understanding metabolic regulation of Th17 cells in uveitis.

## Key findings

- Metabolic pathways influence Th17 cell activation and differentiation.
- Disruption of Th17/Treg balance contributes to autoimmune diseases like uveitis.
- Targeting metabolic checkpoints may offer new treatment options for uveitis.

## Abstract

The disruption of the balance between helper T cells (Th17) and regulatory T cells (Tregs) is associated with various autoimmune diseases. Th17 cells contribute to inflammation, whereas Tregs play a crucial role in suppressing autoimmunity. Th17 cells are central to the pathogenesis of autoimmune diseases, with specific metabolic pathways, enzymes, signaling pathways, and transcription factors acting as key checkpoints that influence T cell differentiation and immune responses. This review aims to summarize recent advances in understanding the role of Th17 cells and the Th17/Treg immune balance in the pathogenesis of uveitis, focusing on the impact of metabolic reprogramming on the activation, differentiation, and effector functions of T cells. Understanding the regulators of key metabolic checkpoints offers promising prospects for the treatment of autoimmune diseases, including Th17-mediated uveitis.