炎症
固有层
模式识别受体
先天免疫系统
免疫学
免疫系统
生物
发病机制
肠粘膜
免疫
炎症性肠病
癌变
粘膜免疫学
受体
信号转导
疾病
癌症
医学
细胞生物学
上皮
病理
内科学
生物化学
遗传学
作者
Masayuki Fukata,Moshe Arditi
摘要
Recognition of microorganisms by pattern-recognition receptors (PRRs) is the primary component of innate immunity that is responsible for the maintenance of host–microbial interactions in intestinal mucosa. Dysregulation in host–commensal interactions has been implicated as the central pathogenesis of inflammatory bowel disease (IBD), which predisposes to developing colorectal cancer. Recent animal studies have begun to outline some unique physiology and pathology involving each PRR signaling in the intestine. The major roles played by PRRs in the gut appear to be the regulation of the number and the composition of commensal bacteria, epithelial proliferation, and mucosal permeability in response to epithelial injury. In addition, PRR signaling in lamina propria immune cells may be involved in induction of inflammation in response to invasion of pathogens. Because some PRR-deficient mice have shown variable susceptibility to colitis, the outcome of intestinal inflammation may be modified depending on PRR signaling in epithelial cells, immune cells, and the composition of commensal flora. Through recent findings in animal models of IBD, this review will discuss how abnormal PRR signaling may contribute to the pathogenesis of inflammation and inflammation-associated tumorigenesis in the intestine.
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