Psoriasis is a chronic inflammatory autoimmune skin disease characterized by erythematous plaques covered with silvery-white scales, often accompanied by systemic complications such as psoriatic arthritis and cardiovascular diseases. The occurrence and progression of this disease are related to the IL-23/IL-17 axis and involve aberrant activation and interactions of multiple immune cells, including keratinocytes, dendritic cells, Th17 cells, and neutrophils, with genetic predispositions and environmental triggers. Currently, psoriasis remains incurable. Therapeutic strategies that primarily focus on immunosuppression, anti-inflammation, and palliative care can only control and delay disease progression. These strategies face challenges relating to cost, safety, efficacy and precision of targeting. Future research should prioritize individualized treatment, immune tolerance induction, and microbiome modulation to achieve long-term disease control and potential cure. This review is primarily focused on the progress and prospects of the pathogenesis and therapies for psoriasis, aiming to provide new insights for individualized treatment in the future.

Autoimmune diseases (ADs) are a group of inflammatory disorders triggered by aberrant immune responses against autoantigens and the breakdown of immune tolerance. Current therapeutic strategies, such as glucocorticoids and immunosuppressants, exert largely non-specific immunomodulation and are frequently associated with substantial adverse effects upon long-term administration. As such, these approaches are often insufficient to re-establish immune homeostasis. In recent years, regulatory T cell (Treg)-based therapeutics have undergone rapid advancement, with continuously updated therapeutic modalities broadening the application boundary of immune tolerance intervention. This review comprehensively outlines the progress of Treg-based therapeutics, spanning from fundamental biological research to translational applications in autoimmune diseases. We describe the developmental characteristics, suppressive machinery, and heterogeneity of Tregs, and highlight the preclinical and clinical advancements of diverse Treg therapeutic modalities, including polyclonal and antigen-specific Tregs, TCR-engineered Tregs, and CAR-Tregs. Furthermore, we emphasize current optimization strategies for enhancing Treg stability, antigen specificity, and in vivo fitness within inflammatory microenvironments. Additionally, we objectively address the major translational bottlenecks of Treg therapy and provide future perspectives to facilitate the clinical implementation of Treg-based immunotherapies for autoimmune diseases.