Research Progress on Th17/Treg Cell Imbalance in Epileptic Seizures

Abstract

Epilepsy is associated with widespread neurological circumstances due to aberrant neuronal discharges in the brain, which have significant adverse effects on patient's quality of life and increase their risk of death. Immune imbalance, particularly disruption of the Th17/Treg cell balance, has gained increasing attention in the pathophysiology of epilepsy as our understanding of neuroimmune interactions improves. This paper examines the potential therapeutic effects and thoroughly discusses the processes by which the Th17/Treg cell imbalance contributes to the development of epilepsy. The primary emphasis is on the mechanism by which this imbalance impairs blood-brain barrier integrity, neuroinflammation, and other elements. On the therapeutic front, targeting the Th17/Treg axis for immune regulation-through approaches such as ketogenic diets, nanomaterials, and gene editing-shows promising prospects for restoring immune balance. By furthering our knowledge of the connection between Th17/Treg cell imbalance and epilepsy etiology, this work offers a crucial theoretical foundation for creating innovative immunotherapy approaches.

Keywords: Th17/Treg cell balance; epilepsy; immune regulation; neuroimmune regulation; neuroinflammation.

Figure 1

CD4⁺ T cells differentiate into two subtypes, Th17 cells and regulatory T (Treg) cells, under the regulation of different environmental factors and cytokines. The differentiation of Th17 cells is stimulated and regulated by pro-inflammatory cytokines, such as interleukin (IL)-6, IL-1β, and IL-23. They primarily secrete cytokines, such as IL-17, IL-21, IL-22, interferon-γ (IFN-γ), and granulocyte-macrophage colony-stimulating factor (GM-CSF), which play a crucial role in tissue inflammatory responses by promoting the recruitment of immune cells and the release of inflammatory factors in tissues, thereby exacerbating inflammatory pathological processes. In contrast, the differentiation of Treg cells is supported by the regulation of transforming growth factor-β (TGF-β) and the expression of the forkhead box protein 3 (FOXP3) gene. These cells primarily secrete inhibitory molecules, such as IL-10, granzyme B, perforin, IL-35, and TGF-β. These molecules help maintain immune homeostasis in the body by inhibiting the activation of effector T cells, reducing the release of inflammatory factors, and regulating the balance, thereby preventing excessive inflammatory responses and the development of autoimmune diseases. Created in BioRender. MU, l. (2025) https://BioRender.com/ahykxiv.