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Endocytosis and transcytosis of gliadin peptides
Molecular and Cellular Pediatrics Pub Date : 2016-02-16 , DOI: 10.1186/s40348-015-0029-z
M Vittoria Barone 1, 2 , K Peter Zimmer 3
Affiliation  

BackgroundCeliac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Some gliadin peptides are not digested by intestinal proteases and can have different biological effects. Gliadin peptides can induce innate and adaptive T cell-mediated immune responses. The major mediator of the stress and innate immune response to gliadin peptides (i.e., peptides 31–43 and 31–55) is the cytokine interleukin-15 (IL-15). Other peptides such as the 33 mer containing the P57–68 sequence, after tissue transglutaminase deamidation, are well presented to T cell in the intestine and can induce an adaptive immune response.FindingsIn this paper, we review the recent studies on the digestion of gliadin and the peptides released by the digestion process. We will also discuss the mechanisms responsible for the internalization and transcytosis of indigested gliadin peptides in the intestinal epithelium.ConclusionsGliadin is not completely digested by the intestinal proteases producing bioactive peptides that have different biological effects. These peptides are internalized in the cells by an active process of endocytosis and can traverse the intestinal mucosa with different kinetics and immunological effects. In vivo findings will also be discussed.

中文翻译:

麦醇溶蛋白肽的内吞作用和转胞吞作用

背景乳糜泻 (CD) 是一种常见的炎症性肠道疾病,具有遗传背景,由含麦醇溶蛋白的食物引起。一些麦醇溶蛋白肽不会被肠道蛋白酶消化,可能会产生不同的生物学效应。麦醇溶蛋白肽可以诱导先天性和适应性 T 细胞介导的免疫反应。对麦胶蛋白肽(即肽 31-43 和 31-55)的应激和先天免疫反应的主要介质是细胞因子白细胞介素 15 (IL-15)。其他肽,如含有 P57-68 序列的 33 mer,在组织转谷氨酰胺酶脱酰胺后,可以很好地呈递给肠道中的 T 细胞,并可以诱导适应性免疫反应。 研究结果在本文中,我们回顾了最近关于麦胶蛋白消化的研究以及消化过程释放的肽。我们还将讨论负责肠上皮中未消化的麦胶蛋白肽内化和转胞吞作用的机制。结论麦胶蛋白未被肠道蛋白酶完全消化,产生具有不同生物学效应的生物活性肽。这些肽通过积极的内吞过程被内在细胞内,并且可以以不同的动力学和免疫学作用穿过肠粘膜。还将讨论体内发现。这些肽通过积极的内吞过程被内在细胞内,并且可以以不同的动力学和免疫学作用穿过肠粘膜。还将讨论体内发现。这些肽通过积极的内吞过程被内在细胞内,并且可以以不同的动力学和免疫学作用穿过肠粘膜。还将讨论体内发现。
更新日期:2016-02-16
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