炎症性肠病(IBD)是一种非可控性慢性炎症，易恶变为结肠癌，其中树突状细胞介导的粘膜免疫发挥了重要作用。前期研究我们通过蛋白组学和基因组学方法，在蛋白和转录水平均发现丝氨酸/苏氨酸受体激酶结合蛋白MAWBP在UC患者肠粘膜中显著低表达，且与UC炎症程度呈负相关，预实验发现在体外炎症-肿瘤细胞模型中过表达MAWBP可抑制炎症因子和癌基因，调控树突状细胞及抗原递呈细胞的相关基因。因此我们推断MAWBP可能通过调控树突状细胞来发挥抑制炎症和肿瘤的作用，本项目拟在体内MAWBP-/-小鼠模型、AOM/Il10-/-炎症-肿瘤动物模型和临床样本中进一步证实MAWBP的功能和机制，通过流式细胞术、电镜技术、磁珠分选和qPCR等检测MAWBP对树突状细胞成熟、模式识别受体、T淋巴细胞增殖、Th细胞分化、炎症肿瘤指标及信号通路等的影响，探讨MAWBP通过介导树突状细胞对IBD炎症-肿瘤进程的负向调控作用。

Inflammatory bowel disease (IBD) is a kind of nonresolving, non-specificity chronic inflammation, a precancerouse lesion, the mucosal immune regulated by dendritic cells takes critical part in the development of IBD. We have performed proteomic analysis and genomics analysis,which indicate that Serine/threonine kinase receptor-binding protein MAWBP was significantly down-regulated in UC intestinal biopsy compared with normal control both in the protein level and mRNA level (Fig. 3), we also found that MAWBP was negatively correlated with the inflammatory degree of UC (Fig. 2). Further more, we did the realtime PCR on the PBMCs from IBD patients and healthy control, MAWBP and MAWD were significantly down-regulated in UC PBMCs compared with healthy control (Fig. 4). Then we did the pre-experiment and found that overexpressed MAWBP in inflammatory-cancer cells model can regulate dentritic cells and antigen presenting cells (Fig. 1), inhibit a large group of cytokines and oncogenes in vitro. Therefore, we deduce that MAWBP could inhibit inflammation and cancer via regulating dendritic cells. In this project, we will verify the role of MAWBP through MAWBP-/-mice, AOM/Il10-/-infammatory-cancer animal model and patients’ samples in vivo. We will detect the role of MAWBP in maturation of dendritic cell, pattern recognition receptors, T lymphocyte proliferation, Th cell differentiation, inflammation index, cancer and pathway with flow cytometry, electron microscopy, MACS MicroBeads and qPCR et al, to investigate the negative role of MAWBP in the process of inflammation-cancer in IBD through regulating dendritic cells.