In summary, we propose a novel mechanism by which CCL5 promotes the differentiation of Th17 cells and the expression of LFA-1 protein on the surface of Th17 cells in mice with PD by activating LCK and ZAP70 proteins in Th17 cells, leading to the infiltration of the SNpc by Th17 cells and inducing neuroinflammation in DA neurons and their death (Figure 8). This evidence concerns the gene ITGAL and Parkinson disease.