炎症性肠病的粘膜免疫学

G. Degasperi
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引用次数: 1

摘要

炎症性肠病(IBD)包括两种主要表型,克罗恩病和溃疡性结肠炎,它们具有不同的临床特征和免疫反应谱。肠道免疫反应失调与促炎细胞因子分泌升高是IBD的一个标志。在本章中,我们将描述参与IBD发病机制的先天免疫和适应性免疫细胞。先天淋巴样细胞以及树突状细胞、中性粒细胞、巨噬细胞、B细胞和T细胞,包括Th1和Th2、Th9和Th17细胞将在这种情况下被特异性表征。这些细胞的交叉对话和细胞因子介导的调控,重点是细胞因子IL-17, IL-22和IL-23也将强调。固有层。这些抗原可以被TLR识别或被M细胞捕获。免疫细胞暴露于腔内内容物诱导TCD4 +激活、分化和炎症细胞因子释放以及中性粒细胞募集。iga活化菌参与了Fc α RI诱导的炎症反应。几个环境因素(饮食、遗传、生活方式)可以调节溃疡性结肠炎的微生物群组成和免疫细胞的激活;
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mucosal Immunology in the Inflammatory Bowel Diseases
Inflammatory bowel disease (IBD) includes two major phenotypes, Crohn’s disease and ulcerative colitis, which have different clinical characteristics and immune response profiles. Dysregulation of the intestinal immune response with elevated secretion of proinflammatory cytokines is a hallmark of IBD. In this chapter, we will characterize the cells of the innate and adaptive immunity involved in the pathogenesis of IBD. Innate lymphoid cells as well as dendritic cells, neutrophils, macrophages, B cells and T cells, including Th1 and Th2, Th9 and Th17 cells will be specifically characterized in this scenario. The cross talks and cytokine-mediated regulation of these cells with emphasis on cytokines IL-17, IL-22 and IL-23 will also be emphasized. propria. These antigens can be recognize by TLR or captured by M cells. The exposure of immune cells to the luminal content induces TCD4 + activation, differentiation and inflammatory cytokine release as well as neutrophil recruitment. IgA-opsonized bacteria contributes to the inflammation induced by Fc α RI. Several environmental factors (diet, genetics, lifestyle) can modulate the microbiota composition and the activation of immune cells in the Ulcerative Colitis;
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