Tumor cells induced-M2 macrophage favors accumulation of Treg in nasopharyngeal carcinoma.

Tumor-associated macrophage (TAM) is major component of tumor immune related inflammation and plays a crucial role in tumor immune escape. However, there have been no studies reported the relationship of TAM and immunosuppressive cell regulatory T cell (Treg) in NPC. This study is to discuss the interaction of TAM and Treg in NPC. In the present study, immunopathological assays demonstrated that M2 macrophage increased in NPC tissues. M2 macrophage had a positive correlation with aberrantly increased Foxp3+ Treg in NPC tissues. High density M2 macrophage and high density Treg predicted poor survival of NPC patients. In vitro studies using tumor cells co-cultured with monocyte indicated that tumor cells could induce monoctye into M2 macrophage via TGF-β1 and IL-10. Tumor cells induced-M2 macrophage could induce the chemotaxis of Treg and increased the percent of Treg in PBMC. Our results proved that NPC cells induced M2 macrophage via TGF-β1 and IL-10, and tumor cells induced-M2 macrophage could favor accumulation of Treg by conversion and chemotaxis.