免疫和炎症构成肿瘤微环境的两大核心，但两者之间关系并不清楚。髓源抑制性细胞（myeloid derived suppressor cell，MDSC）和调节性T细胞（regulatory T cell，Treg）等抑制性细胞趋化至肿瘤部位可抑制炎症，而非介导肿瘤免疫逃逸；肥大细胞则通过对MDSC和Treg的调节，介导免疫和炎症的对话；作为肿瘤微环境中基本信号通路的Toll样信号可以直接调节免疫和炎症，并通过微颗粒途径精细调控肿瘤炎症的稳定。不管肿瘤炎症和免疫的关系如何复杂而交错，一般认为，肿瘤微环境的抗肿瘤免疫和炎症呈现出一种负相关关系，即在肿瘤的早期，免疫反应较强而炎症较弱；但在肿瘤的后期，免疫反应较弱而炎症较强。

Immune response and inflammation composes two cores of tumor microenvironment. However the relationship between them remains elusive. Studies corroborate the idea that the mission of myeloid derived suppressor cells (MDSCs) and regulatory T cells (Tregs) that migrate to tumor sites is to suppress inflammation rather than mediate tumor immune evasion. Mast cells, however, mediate the crosstalk of immune response and inflammation by regulating MDSCs and Tregs. In addition, Toll-like signaling, as the basic signaling pathway in tumor microenvironment, may directly regulate immune response and inflammation, maintaining inflammatory homeostasis through microparticle pathways. Despite the very complex relationship between immune response and inflammation, we suggest that antitumor immune response and inflammation are negatively correlated and time dependent. At the early stage of tumor, antitumor immune responses are dominant. Later, the bias favors inflammation in tumor microenvironment.

国家自然科学基金资助项目(No.30871020)；新世纪大学优秀人才计划资助项目(No.NCET-08-0219)；国家自然科学基金国际合作项目(No.30911120482)