<p>Parkinson’s disease (PD), the second most common neurodegenerative disorder, is characterized by progressive dopaminergic neuron loss in the substantia nigra and α-synuclein aggregation. Emerging evidence highlights the significant role of neuroimmune crosstalk in PD pathogenesis, particularly the interactions between microglia and infiltrating T cells. Disruption of the blood–brain barrier in PD facilitates infiltration of peripheral CD4 + and CD8 + T cells into the central nervous system. Activated CD8 + T cells exert direct neurotoxicity by releasing granzymes, perforin, and proinflammatory cytokines (e.g., TNF-α, IFN-γ), while CD4 + T cell subsets exhibit dual roles. Proinflammatory Th1/Th17 cells exacerbate neuroinflammation, Treg cells and Th2 cells, on the other hand, play a role in suppressing inflammation. Meanwhile, activated microglia secrete cytokines to recruit T cells and activate them through MHC-mediated antigen presentation. Pro-inflammatory T cells, in turn, influence activated microglia, establishing a self-perpetuating cycle of chronic neuroinflammation, ultimately leading to neurodegeneration. These findings highlight the crucial role of neuroimmune interactions in PD progression and suggest potential therapeutic strategies, including targeted depletion or functional inhibition of neurotoxic T cells, prevention of their infiltration into the central nervous system, enhancement of Treg function, modulation of pro-inflammatory microglial activation, etc.</p>