The role of T cells in the treatment of Parkinson’s disease

Current pharmacological treatment of Parkinson's disease (PD) predominantly employs dopaminergic agents aimed at enhancing cerebral dopamine levels. While these therapeutic strategies provide symptomatic relief, their palliative nature is frequently associated with dose-dependent complications, including gastrointestinal disturbances, emetic symptoms, and motor complications such as dyskinesia. Moreover, the honeymoon period of drugs has greatly limited their clinical application. The multifactorial etiology of PD continues to challenge researchers, yet substantial evidence implicates α-synuclein as a critical pathogenic mediator. Emerging findings suggest that dysregulated neuroimmune interactions constitute a fundamental mechanism in PD progression, where chronic immune activation appears particularly detrimental to neuronal survival. Notably, neuroinflammatory cascades coupled with compromised blood-brain barrier (BBB) integrity create a self-perpetuating cycle of neural degeneration, wherein α-synuclein-specific T cells exacerbate disease pathology while regulatory T cell populations demonstrate potential immunomodulatory capacities. This review systematically examines the mechanistic interplay involving neuroinflammatory cascades, BBB compromise, central nervous system (CNS) immunoregulation, and T lymphocyte subpopulations (including regulatory T cells) in the pathogenesis of PD. By synthesizing current evidence, we aim to establish a conceptual framework supporting the investigation of cellular immunity-based therapies for PD.