Fig. 1

Molecules from the endometriotic lesion recruit macrophages. (A) MCP-1 and RANTES in the endometriotic lesion act as attractants to mediate the macrophage recruitment. (B) CCL-2 and CSF-1 secreted from nerve fibers recruit the macrophages into the endometriotic milieu. The CCL-2-mediated recruitment also polarizes the macrophages toward M2 phenotypes. (C) Sema3A/NRP-1 signaling guides the macrophages to the hypoxic microenvironment and regulates the polarization of macrophages toward M2 phenotype. CCL-2: chemokine (C–C motif) ligand 2 or monocyte chemoattractant protein 1 (MCP-1); RANTES: C–C chemokine, regulated on activation, normal T cell expressed and secreted; CCR2: C–C chemokine receptor type 2; CSF-1: colony-stimulating factor 1; Sema3A: semaphorin 3A; NRP-1: neuropilin-1; PlexinA1/A4: plexinA1/A4 receptor; VEGFR: vascular endothelial growth factor receptor; M1: classical activated macrophage; M2: alternatively activated macrophage