CCR2 and Parkinson disease: Moreover, although CD11b+CD45hi-infiltrated IMs decreased significantly in CCR2−/− PD mice compared with control mice, CCR2 knockout did not result in significantly decreased IMs in RBP-JcKO PD mice (Figures 4C, D), indicating that myeloid-specific RBP-J deficiency alleviated DA neurodegeneration independent of CCR2+ monocyte recruitment.