Inflammation in the Intestinal Tract: Pathogenesis and Treatment
Inflammation in the Intestinal Tract: Pathogenesis and Treatment
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DOI：
10.1159/000235851
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发表时间：
2009-01-01
影响因子：
2.3
通讯作者：
Blumberg, Richard S.
中科院分区：
文献类型：
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作者：
Blumberg, Richard S.
在过去的十年中，一个主要的假说已经出现了炎症性肠病（IBD）的发病机制。该假说提出IBD代表了对源自遗传易感宿主中肠道微生物群的抗原的失调的粘膜免疫应答，所述抗原最初源自先天免疫异常，导致源自CD 4 + T细胞的过度促炎细胞因子（辅助T细胞1，辅助T细胞2，和T-辅助细胞17细胞因子）的作用超过通常与耐受性和源自T-调节细胞的免疫调节相关的应答。鉴于遗传易感性已越来越多地被认为影响先天性和适应性免疫的调节、肠上皮细胞生理屏障功能以及抗原通过这种功能障碍的屏障功能进入粘膜免疫系统的潜在不适当途径，理解IBD病理生理学的关键点是理解与肠免疫系统相关的免疫调节途径，因为它们适用于IBD。因此，与先天性和适应性免疫相关的免疫遗传途径、由先天性和适应性免疫细胞分泌的细胞因子、与炎症相关的上皮因子和白细胞因子以及调节白细胞募集的内皮上的结构定义了可能适合IBD治疗操作的潜在途径。版权所有（C）2009 S. Karger AG，巴塞尔
Over the past decade a major hypothesis has emerged for the etiopathogenesis of inflammatory bowel disease (IBD). This hypothesis proposes that IBD represents a dysregulated mucosal immune response to antigens derived from the commensal microbiota in a genetically susceptible host that initially derives from innate immune abnormalities leading to an excessive proinflammatory cytokine derived from CD4+ T cells (T-helper 1, T-helper 2, and T-helper 17 cytokines) over and above the response that is normally associated with tolerance and immunoregulation derived from T-regulatory cells. Given that the genetic predisposition has increasingly been recognized to affect the regulation of innate and adaptive immunity, intestinal epithelial cell physiologic barrier function and the potential inappropriate access of antigens to the mucosal immune system through this dysfunctional barrier function, a key point in understanding IBD pathophysiology is to understand the immunoregulatory pathways associated with the intestinal immune system as they apply to IBD. Therefore, immunogenetic pathways associated with innate and adaptive immunity, the cytokines secreted by innate and adaptive immune cells, the epithelial factors and leukocyte factors that are associated with inflammation and structures on the endothelium that regulate the recruitment of leukocytes define potential pathways that may be amenable to therapeutic manipulation in IBD. Copyright (C) 2009 S. Karger AG, Basel