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本文引用的文献

1
SMAD4 TGF-β-independent function preconditions naive CD8+ T cells to prevent severe chronic intestinal inflammation.SMAD4 的 TGF-β 非依赖性功能使初始 CD8+ T 细胞做好准备,以防止严重的慢性肠道炎症。
J Clin Invest. 2022 Apr 15;132(8). doi: 10.1172/JCI151020.
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The Burden of Inflammatory Bowel Disease in Europe in 2020.2020 年欧洲炎症性肠病负担
J Crohns Colitis. 2021 Sep 25;15(9):1573-1587. doi: 10.1093/ecco-jcc/jjab029.
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A guide to histomorphological evaluation of intestinal inflammation in mouse models.小鼠模型肠道炎症的组织形态学评估指南
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4
Smad4 deficiency in T cells leads to the Th17-associated development of premalignant gastroduodenal lesions in mice.T 细胞中 Smad4 的缺失导致小鼠胃十二指肠前恶性病变中与 Th17 相关的发展。
J Clin Invest. 2011 Oct;121(10):4030-42. doi: 10.1172/JCI45114. Epub 2011 Sep 1.
5
Smad4 signalling in T cells is required for suppression of gastrointestinal cancer.T细胞中的Smad4信号传导是抑制胃肠道癌症所必需的。
Nature. 2006 Jun 22;441(7096):1015-9. doi: 10.1038/nature04846.
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Blocking Smad7 restores TGF-beta1 signaling in chronic inflammatory bowel disease.阻断Smad7可恢复慢性炎症性肠病中的TGF-β1信号传导。
J Clin Invest. 2001 Aug;108(4):601-9. doi: 10.1172/JCI12821.

利用骨髓移植模型探讨传统CD8αβ+ T细胞和CD4+ T细胞在肠道免疫病理学中的作用

Addressing the Role of Conventional CD8αβ+ T Cells and CD4+ T Cells in Intestinal Immunopathology Using a Bone Marrow-Engrafted Model.

作者信息

Aoudi Amneh, Labiad Ossama, Igalouzene Ramdane, Mejri Ousséma, Sanchez Maxime, Soudja Saïdi

机构信息

Tumor Escape Resistance and Immunity Department, Cancer Research Center of Lyon (CRCL), Lyon, France.

INSERM U1052, CNRS UMR 5286, Lyon, France.

出版信息

Bio Protoc. 2024 Feb 20;14(4):e4934. doi: 10.21769/BioProtoc.4934.

DOI:10.21769/BioProtoc.4934
PMID:38405082
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10883888/
Abstract

Inflammatory bowel disease (IBD) is characterized by an aberrant immune response against microbiota. It is well established that T cells play a critical role in mediating the pathology. Assessing the contribution of each subset of T cells in mediating the pathology is crucial in order to design better therapeutic strategies. This protocol presents a method to identify the specific effector T-cell population responsible for intestinal immunopathologies in bone marrow-engrafted mouse models. Here, we used anti-CD4 and anti-CD8β depleting antibodies in bone marrow-engrafted mouse models to identify the effector T-cell population responsible for intestinal damage in a genetic mouse model of chronic intestinal inflammation. Key features • This protocol allows addressing the role of CD4+ or CD8αβ+ in an engrafted model of inflammatory bowel disease (IBD). • This protocol can easily be adapted to address the role of other immune cells or molecules that may play a role in IBD.

摘要

炎症性肠病(IBD)的特征是针对微生物群的异常免疫反应。众所周知,T细胞在介导病理过程中起关键作用。评估每个T细胞亚群在介导病理过程中的作用对于设计更好的治疗策略至关重要。本方案介绍了一种在骨髓移植小鼠模型中鉴定导致肠道免疫病理的特定效应T细胞群体的方法。在这里,我们在骨髓移植小鼠模型中使用抗CD4和抗CD8β耗竭抗体,以在慢性肠道炎症的基因小鼠模型中鉴定导致肠道损伤的效应T细胞群体。关键特性 • 本方案允许在炎症性肠病(IBD)移植模型中探讨CD4+或CD8αβ+的作用。 • 本方案可轻松调整,以探讨可能在IBD中起作用的其他免疫细胞或分子的作用。