Glioblastoma multiforme (GBM) is a highly invasive cancer that is characterized by changes in cerebral vessels and the gradual invasion of surrounding tissues along the perivascular space [1, 2]. In the last years, several immune regulators have been shown to contribute to GBM progression as immunossupressive mechanisms, including recruitment of tumor-associated macrophages (TAMs) and changes of the expression patterns of cytokines that modulate the anti-tumor T cell responses [3–6]. However, the origin of these initial mechanisms underlying the suppression of anti-tumor immune responses around the blood vessel, where GBM initiates and progresses, are poorly understood. Previous works suggest that glioblastoma cells can differentiate into cells of tumor vessels, providing a means of tumor vascularization ; and that the tumorogenic phenotype can be transferred from the tumor cell to host cells around the blood vessels during GBM progression [8, 9]. Thus, to better understand these processes, it is essential to determine the consequences of possible interactions between cancer cells and cells in the perivascular compartments.