کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8368456 1542798 2017 16 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Cells of the innate and adaptive immunity and their interactions in inflammatory bowel disease
ترجمه فارسی عنوان
سلول های ایمنی ذاتی و سازگاری و تعاملات آنها در بیماری التهابی روده
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی، ژنتیک و زیست شناسی مولکولی (عمومی)
چکیده انگلیسی
Inflammatory bowel disease (IBD) is a group of chronic inflammatory conditions of the gastrointestinal tract that includes two major phenotypes, Crohn's disease and ulcerative colitis that are characterized by different clinical features and different course of the immune response. The exact aetiology of IBD still remains unknown, although it is thought that the diseases result from an excessive immune response directed against microbial or environmentally derived antigens which can be triggered by the disruption of the intestinal epithelial barrier integrity. In this review we present immune mechanisms and interactions between cells of the immune system and tissue environment that contribute to the development and progression of IBD in humans. Since dysregulation of the intestinal immune response is a hallmark of chronic inflammatory conditions, we characterize cells of the innate and adaptive immunity involved in the pathogenesis of IBD and their cross-talks. We describe various subclasses of recently discovered innate lymphoid cells, as well as dendritic cells, macrophages and T cells, including Th17, Th22 and T regulatory cells, present in the intestinal lamina propria and cytokine-mediated regulation of the immune response in IBD, highlighting the role of IL-22 and IL-17A/IL-23 axis. Insights into novel therapeutic modalities targeting certain elements of the immune pathways important for the pathogenesis of IBD have been also shortly presented.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Advances in Medical Sciences - Volume 62, Issue 1, March 2017, Pages 1-16
نویسندگان
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