부산대학교 도서관

Glioblastoma (GBM) is the most common primary malignant tumor derived from glial cells. Because complete surgical resection is difficult and very few drugs are approved for GBM treatment, further study is urgently needed to elucidate the pathology of GBM. CCR4 is a chemokine receptor that regulates the migration of regulatory T cells (Tregs) and Th17 cells. Previous studies in GBM patients reported that the expression levels of CCR4 ligands are upregulated in the tumor, and Tregs and Th17 cells are infiltrated into the tumor tissues. However, the role of CCR4 in GBM pathogenesis is poorly understood. In the present study, we found that CCR4 deficiency and selective inhibition promoted tumor growth of GBM and shortened survival duration. Furthermore, Th17 cell, but not Treg, migration into the brain was suppressed in CCR4-deficient and CCR4 inhibitor-treated mice. Similarly, M1 macrophages were reduced in the brain. Taken together with previous reports showing that Th17 cytokines promoted M1 macrophage polarization, these results suggest that CCR4 plays an inhibitory role in tumor growth of GBM via Th17 cell migration into the brain and subsequent M1 macrophage polarization. In this symposium, we would like to discuss about new strategy for treatment of GBM.