Promoted glioma formation by deficiency of Tumor necrosis factor receptor type II

• Main Authors: Chao-ChiChuang, 莊兆祺
• Other Authors: Shun-Fen Tzeng
• Format: Others
• Language: zh-TW
• Published: 2012
• Online Access: http://ndltd.ncl.edu.tw/handle/92114768752398183486

碩士 === 國立成功大學 === 生命科學系碩博士班 === 100 === Microglia play a critical role in the immune response of central nervous system (CNS). Similar to other neurodegenerative disorders, microglia are accumulated in gliomas. However, the role of microglia in glioma progress and anti-tumor activity is arguable. It has been known that systemic inflammation increases the production of pro-inflammatory cytokines, including interleukin-1 (IL-1) and tumor necrosis factor- (TNF-). These cytokines not only mediate local inflammation in peripheral tissues, but also trigger neuroinflammation in the CNS. The multiple actions of TNF- are derived from the complexity of TNF receptor type I (TNFRI) and type II (TNFRII)-triggered signaling pathways. Our recent findings have showed that intraperitoneal (ip) injection with lipopolysaccharide (LPS) into TNFRII-/- mice (0.5 mg/kg/day) significantly increased CD11b+ microglia/macrophages in the cortex. In addition, progressive C6-glioma cell formed tumor was observed at the implanted site of TNFRII-/- mice brain when compared to that seen in TNFRII+/- mice. We also observed the lower survival rate of TNFRII-/- mice receiving peripheral LPS injection after C6 glioma cells when compared to that detected in wild type (WT) and TNFRII+/- mice. Yet, No different change in the survival rate of TNFRII-/- mice treated with peripheral LPS injection before C6 glioma cell implantation when compared to that observed in WT and TNFRII+/- mice. However, increased tumor volume was observed in TNFRII-/- mice receiving LPS prior to C6 glioma implantation. Together, the results suggest that TNFRII deficiency and microglia activation are positively correlated with enhancement of glioma formation. Key words：TNF receptor type II、lipopolysaccharide、glioma