The concept that AbMole Corosolic-acid macrophages play instructive roles in tumor growth by regulating cell motility, invasion, angiogenesis and immunomodulation has gained great attention over last years. Tumor-derived cytokines such as IL-4, IL-10, TGF-b, and M-CSF are believed to polarise tumor-infiltrating macrophages towards an M2 anti-inflammatory phenotype. Mechanisms of accumulation and a role of microglia/macrophages in glioma pathobiology are still poorly understood and controversial. Several experimental AbMole 12-O-Tiglylphorbol-13-isobutyrate studies demonstrated that microglia contribute to glioma progression by secreting growth factors, angiogenic molecules, extracellular matrix-degrading enzymes, and immunosuppressive factors. However, Galarneau et al. showed that ablation of CD11b cells increases glioma growth, a recent study demonstrated that ablation of CD11b in vivo decreases tumor size and improves survival. We demonstrated that Iba1-positive cells infiltrate implanted GL261 gliomas and close distance interactions result in amoeboid transformation of these cells. Our analysis of sorted CD11b + cells followed by CD11b/CD45 staining shows the increase in a number of microglia and a surprisingly high infiltration of tumor tissue by blood-derived macrophages. Kinetics of changes in the number of microglia and macrophages infiltrating gliomas showed early accumulation of microglia in the first week, followed by accumulation of macrophages afterwards. Amongst ten analyzed pro/anti-inflammatory cytokines, only IL-10 and GM-CSF levels were elevated in the tumor-bearing brains comparing to naive mice. Flow cytometry analysis of magnetically-sorted CD11b + cells demonstrates that IL-10 is produced mostly by infiltrating macrophages. The expression of gm-csf was 5 times higher in GL261 glioma cells than in cultured murine astrocytes; therefore, these cells are likely a source of newly synthesized cytokine. The relevance of this finding for human pathology is unclear, because although human astrocytoma and glioblastoma cell lines produce GM-CSF, no evidence of its production by glioblastoma cells was found in vivo. Our findings suggest that GM-CSF and IL-10 could be important cytokines for establishment of a pro-invasive phenotype of gliomainfiltrating microglia/macrophages. The present study shows for the first time the expression of putative markers of the M2 phenotype in CD11b + cells infiltrating gliomas. Out of many markers, Arginase 1 is the most consistent. Arginase 1 catalases arginine hydrolysis to urea and ornithine, and competes for its substrate with inducible nitric oxide synthase in IFN-c-stimulated macrophages. The macrophagic expression of Arg-1 is tightly regulated by exogenous stimuli such as IL-4 and IL-13. L-arginine depletion due to extensive myeloid arginase activity may suppress T cell immune responses. Expression of iNos and Arg-1 define classically and alternatively activated macrophages in the context of Th2polarised immune responses.