经典型骨髓增殖性肿瘤(MPN)发病率呈逐年上升趋势。其体质性症状是影响患者生活质量的重要因素之一，主要与体内炎症因子分泌调控异常相关。慢性炎症与MPN密切相关，但具体机制有待深入研究。文献报道MPN患者单核细胞血症和肿瘤坏死因子(TNF-α)水平与其预后相关，TNFR2(TNF-α受体)与多种实体肿瘤预后相关，主要通过激活NF-kB通路而促进肿瘤细胞增殖。我们前期研究亦发现MPN患者血清TNF-α水平和细胞表面TNFR2水平均较健康人群明显增高，基于上述研究提出假说：单核细胞通过膜TNF-α与MPN细胞的TNFR2相互作用而激活NF-kB通路参与MPN发生发展。拟通过细胞实验和动物实验探明单核细胞通过mTNF-α/TNFR2/NF-kB通路参与经典型MPN发生的作用机制，并寻找抑制炎症通路的治疗靶点如清除单核细胞药物或TNFR2抑制剂，为阻止MPN的发生发展及改善体质性症状提供新的思路。

Classic myeloproliferative neoplasms present with a tendency of increased incidence. One of crucial factors affecting the quality of life for MPN patients is the constitutional symptoms which are caused mainly by the abnormal release of inflammatory cytokines. Chronic inflammation is closely related to MPN; however, the underlying mechanism deserves further study. Literatures reported that monocytosis and abnormal level of TNF-α are bad prognostic factors for MPN, and researches showed that TNFR2 (TNF-α receptor) were often high expressed in tumor cells and it is related to bad prognosis for tumor because of NF-kB pathway hyperactivation resulting in high proliferation of tumor cells. Our own preliminary results revealed also that MPN patients presented higher level of TNF-α and TNFR2 comparing to that of health control group. Based on results from literatures and our own preliminary experiments, we propose hypothesis: monocyte could implicate in the pathogenesis of classic MPN via the cell interaction between monocyte and MPN cells by recognition between mTNF-α and TNFR2, then it intrigues the hyperactivation of NF-kB which results in high proliferation of MPN tumor cells. This study aims to clarify this underlying mechanism with cell co-culture and animal model and explore the potential remedy of improving MPN by eliminating monocyte or by using TNFR2 inhibitors in order to provide new ideas for preventing MPN progression and improving MPN constitutional symptoms.