In the present study, we found that TLR4 tightly regulated the CD11b+Ly6Chi peripheral expansion and the renal recruitment via the MCP-1 dependent mechanism as deletion of myeloid tlr4 inhibited renal MCP-1 expression and the peripheral and renal CD11b+Ly6Chi population expansion, thereby largely inhibiting M1 proinflammatory macrophage while promoting M2 anti-inflammatory macrophage accumulation in the diseased kidneys of anti-GBM GN. This evidence concerns the gene ITGAM and glioblastoma.