Moutsopoulos Niki M, Wen Jie, Wahl Sharon M
Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4352, United States.
Curr Opin Immunol. 2008 Apr;20(2):234-40. doi: 10.1016/j.coi.2008.04.003. Epub 2008 May 15.
Mechanisms of host defense can form an unwitting alliance with tumor cells to promote tumor progression, invasion, and dissemination to distant sites. By secreting TGF-beta, an immunoregulatory molecule designated for both promoting inflammation and dampening immune responses, the tumor tricks the host into supporting its expansion and survival. TGF-beta not only recruits leukocytes to secrete chemokines, growth factors, cytokines, and proteases in support of a tumor-friendly niche but also in a context-specific manner, incapacitates the emergent immune response. As a profound immunosuppressant, TGF-beta, both directly and through the generation of regulatory T cells, blunts immune surveillance, favoring tumor escape. Collectively, the ability of the tumor to hijack these host defense pathways can tip the balance in favor of the tumor.
宿主防御机制可能会与肿瘤细胞形成一种无意间的联盟，从而促进肿瘤进展、侵袭以及向远处转移。肿瘤通过分泌转化生长因子β（TGF-β）——一种既促进炎症又抑制免疫反应的免疫调节分子——来诱使宿主支持其增殖和存活。TGF-β不仅招募白细胞分泌趋化因子、生长因子、细胞因子和蛋白酶，以营造有利于肿瘤生长的微环境，还能根据具体情况抑制新出现的免疫反应。作为一种强效免疫抑制剂，TGF-β直接或通过生成调节性T细胞来削弱免疫监视，从而有利于肿瘤逃逸。总体而言，肿瘤劫持这些宿主防御途径的能力会使平衡向有利于肿瘤的方向倾斜。
