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Parkinson's disease (PD) is a chronic progressive disease that affects the central nervous system with a variety of symptoms. Although the precise etiology of PD is not yet fully understood, there is evidence to suggest that T cells serve an important role in the pathogenesis of PD. However, how T cells are recruited in the brain tissue remains to be elucidated. The present study utilized human samples from patients with and without PD to investigate the infiltration of T cells in lesions in the central nervous system. A chemically-induced mouse PD model was also used to investigate the roles of T cells in the pathogenesis of PD. Depletion of CD4 + or CD8 + T cells was achieved using neutralizing antibodies. Adhesion molecule levels were assessed by flow cytometry. The results of the study indicated that T cell infiltration was evident in both human and murine samples of PD. Blocking CD4 + or CD8 + T cells attenuated the severity of murine PD. Intercellular adhesion molecule 1 (ICAM1 or CD54) was upregulated in mouse PD compared with controls, and its receptor, lymphocyte function-associated antigen-1 (LFA1) was overexpressed in T cells of the brain in PD mice compared with controls. Furthermore, inhibition of ICAM1 or LFA1 attenuated PD-associated characteristics in mice. In conclusion, the interaction between ICAM1 and LFA1 plays a role in recruiting T cells to the central nervous system to mediate experimental PD.

Interaction between ICAM1 in endothelial cells and LFA1 in T cells during the pathogenesis of experimental Parkinson's disease