RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Animal models of inflammatory bowel disease: novel experiments for revealing pathogenesis of colitis, fibrosis, and colitis-associated colon cancer.
Animal models of inflammatory bowel disease: novel experiments for revealing pathogenesis of colitis, fibrosis, and colitis-associated colon cancer.
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炎症性肠病(IBD)包括克罗恩病和溃疡性结肠炎,是一种终身性疾病,表现为慢性肠道炎症、序贯性纤维化以及结肠炎相关结肠癌(CAC)风险增加。遗传、免疫、环境和微生物因素的联合作用使得确定IBD诱导和持续存在的具体机制变得困难。各种IBD动物模型在基因组学、转录组学、蛋白质组学、微生物组以及新型治疗药物的开发方面,为理解IBD发病机制做出了巨大贡献。尽管基因工程模型等先进技术使IBD的全面研究成为可能,但仍迫切需要开发相关的结肠炎和纤维化体内模型。在此,我们综述了4类急性和慢性肠道炎症、纤维化及CAC的动物模型:化学诱导模型、基因工程模型、T细胞转移模型和自发基因突变模型。
Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is a lifelong disease that manifests with chronic intestinal inflammation, sequential fibrosis, and an increased risk of colitis-associated colon cancer (CAC). The combined effects of genetic, immunological, environmental, and microbial factors render it difficult to determine the specific mechanism underlying the induction and perpetuation of IBD.
Various animal models of IBD have contributed enormously to the understanding of IBD pathogenesis in terms of genomics, transcriptomics, proteomics, microbiome, and drug development of novel therapeutics. Although comprehensive research on IBD has been enabled by advanced technologies, such as genetically engineered models, there is a great need to develop relevant in vivo models of colitis and fibrosis.
Here, we review 4 categories of animal models of acute and chronic intestinal inflammation, fibrosis, and CAC: chemically induced, genetically engineered, T cell transfer, and spontaneous gene mutation models.
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