Compelling evidence showed that the immunologic modulation of Tregs had an inhibitory effect on neuroinflammation leading to the reduction in the motor disorder of PD [22], and TGF-β released from Tregs acted against the MPP+-induced DA neuronal death via TβR-I on microglia [23,24,25], which also supported our results that CA upregulated TGF-β expression accompanied by the decrease in gliosis. Here, TGFBR1 is linked to Parkinson disease.