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开发一种抗原驱动的结肠炎模型,以研究抗原呈递细胞向T细胞呈递抗原的过程。

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells.

作者信息

Rossini Valerio, Radulovic Katarina, Riedel Christian U, Niess Jan Hendrik

机构信息

APC Microbiome Institute, University College Cork.

Division of Gastroenterology and Hepatology, University Hospital Basel.

出版信息

J Vis Exp. 2016 Sep 18(115):54421. doi: 10.3791/54421.

DOI:10.3791/54421
PMID:27684040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5092027/
Abstract

Inflammatory bowel disease (IBD) is a chronic inflammation which affects the gastrointestinal tract (GIT). One of the best ways to study the immunological mechanisms involved during the disease is the T cell transfer model of colitis. In this model, immunodeficient mice (RAG(-/-) recipients) are reconstituted with naive CD4(+) T cells from healthy wild type hosts. This model allows examination of the earliest immunological events leading to disease and chronic inflammation, when the gut inflammation perpetuates but does not depend on a defined antigen. To study the potential role of antigen presenting cells (APCs) in the disease process, it is helpful to have an antigen-driven disease model, in which a defined commensal-derived antigen leads to colitis. An antigen driven-colitis model has hence been developed. In this model OT-II CD4(+) T cells, that can recognize only specific epitopes in the OVA protein, are transferred into RAG(-/-) hosts challenged with CFP-OVA-expressing E. coli. This model allows the examination of interactions between APCs and T cells in the lamina propria.

摘要

炎症性肠病(IBD)是一种影响胃肠道(GIT)的慢性炎症。研究该疾病过程中涉及的免疫机制的最佳方法之一是结肠炎的T细胞转移模型。在这个模型中,免疫缺陷小鼠(RAG(-/-)受体)用来自健康野生型宿主的初始CD4(+) T细胞进行重建。当肠道炎症持续存在但不依赖于特定抗原时,这个模型可以检测导致疾病和慢性炎症的最早免疫事件。为了研究抗原呈递细胞(APC)在疾病过程中的潜在作用,拥有一个抗原驱动的疾病模型是有帮助的,在这个模型中,特定的共生菌衍生抗原会导致结肠炎。因此,已经开发了一种抗原驱动的结肠炎模型。在这个模型中,只能识别OVA蛋白中特定表位的OT-II CD4(+) T细胞被转移到用表达CFP-OVA的大肠杆菌攻击的RAG(-/-)宿主中。这个模型可以检测固有层中APC和T细胞之间的相互作用。

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Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells.开发一种抗原驱动的结肠炎模型,以研究抗原呈递细胞向T细胞呈递抗原的过程。
J Vis Exp. 2016 Sep 18(115):54421. doi: 10.3791/54421.
2
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本文引用的文献

1
Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice.低聚果糖在C57BL/6J小鼠结肠炎的CD4+ CD62L+ T细胞转移模型中发挥肠道抗炎活性。
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Regional specialization within the intestinal immune system.肠道免疫系统的区域专业化。
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Oral tolerance can be established via gap junction transfer of fed antigens from CX3CR1⁺ macrophages to CD103⁺ dendritic cells.口服耐受可以通过 CX3CR1⁺ 巨噬细胞向 CD103⁺ 树突状细胞传递摄取的抗原,通过缝隙连接进行建立。
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Validation of bovine glycomacropeptide as an intestinal anti-inflammatory nutraceutical in the lymphocyte-transfer model of colitis.验证牛糖巨肽作为一种肠道抗炎的营养保健品在结肠炎淋巴细胞转移模型中的作用。
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6
CX3CR1⁺ cells facilitate the activation of CD4 T cells in the colonic lamina propria during antigen-driven colitis.在抗原驱动的结肠炎中,CX3CR1⁺细胞促进结肠固有层中 CD4 T 细胞的激活。
Mucosal Immunol. 2014 May;7(3):533-48. doi: 10.1038/mi.2013.70. Epub 2013 Oct 16.
7
Contributions of dendritic cells and macrophages to intestinal homeostasis and immune defense.树突状细胞和巨噬细胞对肠道稳态和免疫防御的贡献。
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8
Luminal bacteria recruit CD103+ dendritic cells into the intestinal epithelium to sample bacterial antigens for presentation.腔菌招募 CD103+树突状细胞进入肠道上皮细胞,以采样细菌抗原进行呈递。
Immunity. 2013 Mar 21;38(3):581-95. doi: 10.1016/j.immuni.2013.01.009. Epub 2013 Feb 7.
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Changes of the cytokine profile in inflammatory bowel diseases.炎症性肠病细胞因子谱的变化。
World J Gastroenterol. 2012 Nov 7;18(41):5848-61. doi: 10.3748/wjg.v18.i41.5848.
10
CX(3)CR1(+) macrophages support IL-22 production by innate lymphoid cells during infection with Citrobacter rodentium.CX(3)CR1(+) 巨噬细胞在感染柠檬酸杆菌属期间支持先天淋巴细胞产生 IL-22。
Mucosal Immunol. 2013 Jan;6(1):177-88. doi: 10.1038/mi.2012.61. Epub 2012 Aug 1.