A novel strategy against bone invasion of oral cancer

尽管CD 4 +T细胞已被证明在炎症性疾病的微环境中对骨破坏起重要作用，但很少有工作证明这些细胞类型对癌症骨侵袭的贡献。在本研究中，我们研究了口腔癌小鼠模型中调节性T细胞（TCRs）和破骨细胞之间的相互作用机制，以阐明TCRs在口腔癌骨侵袭中的作用。从小鼠口腔癌模型的肿瘤中分离纯化T细胞，然后与骨髓细胞共培养。测定分泌的抗酒石酸酸性磷酸酶（TRACP）5 b作为破骨细胞数量的标志物。在肿瘤来源的THP和骨髓细胞的共培养物中观察到破骨细胞来源的TRACP 5 b的衰减，并且这种TRACP 5 b的衰减通过细胞毒性T淋巴细胞相关抗原-4（CTLA-4）的中和而改善。

Despite CD4+T cells have been demonstrated to play an important role for bone destruction in the microenvironment of inflammatory diseases, very little work has been done to demonstrate the contribution of these cell types to cancer bone invasion. In the present study, we investigated the mechanism of interaction between regulatory T cells (Tregs) and osteoclasts in a murine model of oral cancer to elucidate the role of Tregs in the bone invasion of oral cancer. Tregs were purified from the tumor of mouse oral cancer model and then cocultured with bone marrow cells. Secreted tartrate-resistant acid phosphatase (TRACP) 5b was determined as a marker of osteoclast number. Attenuation of osteoclast-derived TRACP5b was observed in the coculture of tumor derived Tregs and bone marrow cells, and this attenuation of TRACP5b was ameliorated by neutralization of cytotoxic T-lymphocyte-associated antigens-4 (CTLA-4).