Fig 2: CCL5 affected Th17 cell differentiation and function in PD by activating LCK and ZAP70 in Th17 cells. CCL5 activates LCK and ZAP70 by stimulating the Th17 cell surface receptor CCR5, which in turn promotes the expression of LFA-1 on the Th17 surface and increases Th17 differentiation. The influence of CCL5 on Th17 cells can promote an increase in the Th17 cell proportion and infiltration into the SNpc, induce neuroinflammation and death of DA neurons, and participate in PD-related pathology.

Fig 3: CCL5 promoted Th17 cell differentiation and LFA-1 expression by activating LCK and ZAP70. (A) Flow cytometry and FlowJo software were used to analyze peripheral PBMCs from mice. The proportions of IL-17A+, IL-17A+ and LFA-1+, IL-17A+ and pLCK+, IL-17A+ and pZAP70+ cells among CD4+ cell populations were calculated n = 5 per group. (B) Naive CD4+ T cells that were cultured in vitro were induced to differentiate into Th17 cells, which were treated with CCL5 or PBS. After 3 days, LFA-1, pLCK, pZAP70, total LCK, total ZAP70 and Rorγt levels were measured by Western blot analysis and quantified using ImageJ n = 3 per group. Data are presented as the means ± SEMs. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001.