Macrophages are able to polarize from a basal, naïve state to an M1 or M2 phenotype. M1 pro-inflammatory macrophages are characterized by recognizing and eliminating abnormal cells, while M2 anti-inflammatory macrophages are characterized by tissue repair and healing. Polarization toward these phenotypes is induced by the cellular release of specific cytokines. In a tumorigenic environment, cancer cells manipulate the polarization of macrophages by directly releasing cytokines to stop the M1 attack response, and instead induce the M2 phenotype. These hijacked macrophages are called tumor-associated macrophages (TAMs) and are used to sustain an environment that promotes angiogenesis and tumor growth and development. Polarization toward M1 is induced by LPS and IFN-γ cytokines, while polarization toward M2 is induced by IL-4 and IL-13. Experiments were conducted using a murine macrophage cell line (RAW264), murine bone marrow-derived primary macrophages, and a human macrophage cell line (THP-1) to observe cytokine-induced macrophage polarization. Additionally, human glioblastoma cell lines (U87 and T98G) were used to observe the effects of tumor-conditioned media on macrophage polarization in the murine bone marrow-derived primary macrophages and human THP-1 macrophage line. Real-time PCR confirmed the accurate polarization of macrophages treated with M1 and M2-polarizing cytokines, as well as the polarization of macrophages treated with tumor-conditioned media by measuring the mRNA expression of M1 and M2-specific target genes.
Arete: The PLNU Honors Journal