CCR3 and neoplasm: By investigating the potential players in mediating the reduction in gMDSCs via bulk RNA-seq analysis of tumors, we found that αPD1 treatment a) increased the expression of Arginase1, Mrc1 or CD206, and Mgl2—genes associated with immune suppression by MDSCs and tumor-brain interfacial macrophages/microglia (50, –52), b) increased Ccl24 and c) led to a trend toward increased Ccr3, a receptor of Ccl24 involved in eosinophil, T cell, and neutrophil chemotaxis (Fig. 5B).