Exploring the Central Role of the Imbalance between T helper 17 (Th17) and Regulatory T (Treg) Cells in Autoimmune Disease Progression: A review

Immune balance is mainly maintained through coordination between effector and regulatory T cells, especially the Th17 and Treg subsets. These two types perform opposite functions—one drives inflammation while the other limits it—to preserve immune tolerance. When this coordination fails, the system drifts toward autoimmunity. Excessive Th17 activity and a shortage of functional Tregs have been reported in many disorders, but the molecular events behind their instability are still being investigated. Researchers have recently focused on therapeutic methods that might restore this disturbed ratio. The flexible nature of T cells makes such control difficult, since each subset can shift its phenotype depending on signals in the environment. Clinical and laboratory findings show altered Th17/Treg proportions in several autoimmune diseases, including type1 diabetes, lupus, multiple sclerosis, and psoriasis. In diabetic patients, a higher percentage of Tregs often coincides with lower HbAIc and reduced insulin demand, while increased Th17 activity predicts more severe disease. Studies of gene expression also reveal specific chromatin patterns that mark pathogenic Th17 cells. In addition, new approaches such as Treg-based treatments and engineered CAR-Treg cells are being explored to regulate these immune pathways. Altogether, current findings highlight that the Th17/Treg disequilibrium is a core element in autoimmune pathology, and restoring this cellular dialogue is a major target for future immunotherapy.