• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

NOD2 缺陷增加克罗恩病中分泌型 IgA 复合物的逆行运输。

NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn's disease.

机构信息

GIMAP/EA3064, Université de Lyon, CIC 1408 Vaccinology, F42023, Saint-Etienne, France.

R&D Laboratory of the Division of Immunology and Allergy, CHUV, Centre des Laboratoires d'Epalinges, 1066, Epalinges, Switzerland.

出版信息

Nat Commun. 2021 Jan 11;12(1):261. doi: 10.1038/s41467-020-20348-0.

DOI:10.1038/s41467-020-20348-0
PMID:33431850
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7801705/
Abstract

Intestinal microfold cells are the primary pathway for translocation of secretory IgA (SIgA)-pathogen complexes to gut-associated lymphoid tissue. Uptake of SIgA/commensals complexes is important for priming adaptive immunity in the mucosa. This study aims to explore the effect of SIgA retrograde transport of immune complexes in Crohn's disease (CD). Here we report a significant increase of SIgA transport in CD patients with NOD2-mutation compared to CD patients without NOD2 mutation and/or healthy individuals. NOD2 has an effect in the IgA transport through human and mouse M cells by downregulating Dectin-1 and Siglec-5 expression, two receptors involved in retrograde transport. These findings define a mechanism of NOD2-mediated regulation of mucosal responses to intestinal microbiota, which is involved in CD intestinal inflammation and dysbiosis.

摘要

肠上皮内淋巴细胞是分泌型免疫球蛋白 A（SIgA）-病原体复合物向肠相关淋巴组织易位的主要途径。摄取 SIgA/共生复合物对于在黏膜中启动适应性免疫很重要。本研究旨在探讨 SIgA 免疫复合物逆行转运在克罗恩病（CD）中的作用。我们在此报告，与无 NOD2 突变和/或健康个体的 CD 患者相比，NOD2 突变的 CD 患者的 SIgA 转运显著增加。NOD2 通过下调参与逆行转运的两个受体 Dectin-1 和 Siglec-5 的表达，对人源和鼠源 M 细胞中的 IgA 转运具有影响。这些发现定义了 NOD2 介导的对肠道微生物群的黏膜反应的调节机制，该机制涉及 CD 肠道炎症和菌群失调。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/26d70601f056/41467_2020_20348_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/822aed969ef2/41467_2020_20348_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/902a1f73945f/41467_2020_20348_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/c3e754b6028d/41467_2020_20348_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/653fe2a9b901/41467_2020_20348_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/ce4d08622bae/41467_2020_20348_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/26d70601f056/41467_2020_20348_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/822aed969ef2/41467_2020_20348_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/902a1f73945f/41467_2020_20348_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/c3e754b6028d/41467_2020_20348_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/653fe2a9b901/41467_2020_20348_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/ce4d08622bae/41467_2020_20348_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02b7/7801705/26d70601f056/41467_2020_20348_Fig6_HTML.jpg

相似文献

1
NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn's disease.NOD2 缺陷增加克罗恩病中分泌型 IgA 复合物的逆行运输。
Nat Commun. 2021 Jan 11;12(1):261. doi: 10.1038/s41467-020-20348-0.
2
Dectin-1 is essential for reverse transcytosis of glycosylated SIgA-antigen complexes by intestinal M cells.Dectin-1 对于肠道 M 细胞对糖基化 SIgA-抗原复合物的反向转胞吞作用是必需的。
PLoS Biol. 2013 Sep;11(9):e1001658. doi: 10.1371/journal.pbio.1001658. Epub 2013 Sep 17.
3
Nod2 Deficiency Leads to a Specific and Transmissible Mucosa-associated Microbial Dysbiosis Which Is Independent of the Mucosal Barrier Defect.Nod2 缺乏导致特定且可传播的黏膜相关微生物失调，这种失调与黏膜屏障缺陷无关。
J Crohns Colitis. 2016 Dec;10(12):1428-1436. doi: 10.1093/ecco-jcc/jjw095. Epub 2016 May 4.
4
SIgA-Shigella Immune Complexes Interact with Dectin-1 and SIGNR3 to Differentially Regulate Mouse Peyer's Patch and Mesenteric Lymph Node Dendritic Cell's Responsiveness.分泌型免疫球蛋白A-志贺氏菌免疫复合物与脱噬素-1和信号调节蛋白3相互作用，以差异性调节小鼠派尔集合淋巴结和肠系膜淋巴结树突状细胞的反应性。
J Mol Biol. 2017 Jul 21;429(15):2387-2400. doi: 10.1016/j.jmb.2017.05.024. Epub 2017 Jun 3.
5
Selective adherence of IgA to murine Peyer's patch M cells: evidence for a novel IgA receptor.IgA对小鼠派尔集合淋巴结M细胞的选择性黏附：新型IgA受体的证据
J Immunol. 2002 Aug 15;169(4):1844-51. doi: 10.4049/jimmunol.169.4.1844.
6
Induction and rescue of Nod2-dependent Th1-driven granulomatous inflammation of the ileum.诱导并挽救 Nod2 依赖性 Th1 驱动的回肠肉芽肿性炎症。
Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14739-44. doi: 10.1073/pnas.1003363107. Epub 2010 Aug 2.
7
CARD15/NOD2 is required for Peyer's patches homeostasis in mice.CARD15/NOD2 对于维持小鼠派尔集合淋巴结的稳态是必需的。
PLoS One. 2007 Jun 13;2(6):e523. doi: 10.1371/journal.pone.0000523.
8
Cellular and molecular mechanisms underlying NOD2 risk-associated polymorphisms in Crohn's disease.克罗恩病中与NOD2风险相关多态性的细胞和分子机制。
Immunol Rev. 2014 Jul;260(1):249-60. doi: 10.1111/imr.12193.
9
Nod2 Protects the Gut From Experimental Colitis Spreading to Small Intestine.Nod2 保护肠道免受实验性结肠炎向小肠扩散。
J Crohns Colitis. 2020 Jun 19;14(5):669-679. doi: 10.1093/ecco-jcc/jjz196.
10
Targeting of secretory IgA to Peyer's patch dendritic and T cells after transport by intestinal M cells.经肠道M细胞转运后，分泌型IgA靶向派尔集合淋巴结中的树突状细胞和T细胞。
J Immunol. 2004 Mar 1;172(5):3026-33. doi: 10.4049/jimmunol.172.5.3026.

引用本文的文献

1
Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.炎症性肠病中的自噬：免疫、病因及治疗潜力
Front Immunol. 2025 Aug 6;16:1543040. doi: 10.3389/fimmu.2025.1543040. eCollection 2025.
2
Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.与炎症性肠病相关的主要遗传因素及其对肠道通透性的影响：参与肠道炎症。
J Gastroenterol. 2025 Aug 21. doi: 10.1007/s00535-025-02289-x.
3
Gut expression of CD71 and co-localisation with Dec-1 associated with high levels of serum SIgA and disease activity in SpA.

本文引用的文献

1
Anti-commensal IgG Drives Intestinal Inflammation and Type 17 Immunity in Ulcerative Colitis.抗共生 IgG 驱动溃疡性结肠炎的肠道炎症和 17 型免疫。
Immunity. 2019 Apr 16;50(4):1099-1114.e10. doi: 10.1016/j.immuni.2019.02.006. Epub 2019 Mar 12.
2
Colonic epithelial cell diversity in health and inflammatory bowel disease.健康和炎症性肠病中的结肠上皮细胞多样性。
Nature. 2019 Mar;567(7746):49-55. doi: 10.1038/s41586-019-0992-y. Epub 2019 Feb 27.
3
Antigen-presenting ILC3 regulate T cell-dependent IgA responses to colonic mucosal bacteria.
CD71在肠道的表达以及与Dec-1的共定位与脊柱关节炎患者血清SIgA高水平和疾病活动相关。
Sci Rep. 2025 Jun 4;15(1):19517. doi: 10.1038/s41598-025-03532-4.
4
Advancements in the Extraction, Characterization, and Bioactive Potential of Laminaran: A Review.海带的提取、表征及生物活性潜力研究进展：综述
Foods. 2025 May 9;14(10):1683. doi: 10.3390/foods14101683.
5
Selective IgA Deficiency and Aseptic Liver Abscess as Initial Indicators of Crohn's Disease in a Young Woman: A Case Study.选择性IgA缺乏症和无菌性肝脓肿作为一名年轻女性克罗恩病的初始指标：病例研究
Am J Case Rep. 2024 Dec 24;25:e944829. doi: 10.12659/AJCR.944829.
6
Immunoglobulin A Antibodies: From Protection to Harmful Roles.免疫球蛋白A抗体：从保护作用到有害作用
Immunol Rev. 2024 Nov;328(1):171-191. doi: 10.1111/imr.13424. Epub 2024 Nov 23.
7
NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis.NOD2 通过抑制 TYMS/PLK1 信号轴降低黑色素瘤的化疗耐药性。
Cell Death Dis. 2024 Oct 1;15(10):720. doi: 10.1038/s41419-024-07104-8.
8
Role and molecular mechanism of NOD2 in chronic non-communicable diseases.NOD2 在慢性非传染性疾病中的作用和分子机制。
J Mol Med (Berl). 2024 Jun;102(6):787-799. doi: 10.1007/s00109-024-02451-7. Epub 2024 May 14.
9
Intestinal Mucosal Immune Barrier: A Powerful Firewall Against Severe Acute Pancreatitis-Associated Acute Lung Injury via the Gut-Lung Axis.肠道黏膜免疫屏障：通过肠-肺轴抵御重症急性胰腺炎相关性急性肺损伤的强大防火墙
J Inflamm Res. 2024 Apr 10;17:2173-2193. doi: 10.2147/JIR.S448819. eCollection 2024.
10
Gastrointestinal microbiota and metabolites possibly contribute to distinct pathogenicity of SARS-CoV-2 proto or its variants in rhesus monkeys.胃肠道微生物群和代谢物可能导致 SARS-CoV-2 原型或其变体在恒河猴中具有不同的致病性。
Gut Microbes. 2024 Jan-Dec;16(1):2334970. doi: 10.1080/19490976.2024.2334970. Epub 2024 Apr 2.
抗原呈递 ILC3 调节 T 细胞依赖性 IgA 对结肠黏膜细菌的应答。
J Exp Med. 2019 Apr 1;216(4):728-742. doi: 10.1084/jem.20180871. Epub 2019 Feb 27.
4
c-Maf-dependent T cell control of intestinal T17 cells and IgA establishes host-microbiota homeostasis.c-Maf 依赖性 T 细胞控制肠道 T17 细胞和 IgA 从而建立宿主-微生物群的稳态。
Nat Immunol. 2019 Apr;20(4):471-481. doi: 10.1038/s41590-019-0316-2. Epub 2019 Feb 18.
5
Intestinal permeability in physiological and pathological conditions: major determinants and assessment modalities.生理和病理条件下的肠道通透性：主要决定因素和评估方式。
Eur Rev Med Pharmacol Sci. 2019 Jan;23(2):795-810. doi: 10.26355/eurrev_201901_16894.
6
Nod2 influences microbial resilience and susceptibility to colitis following antibiotic exposure.Nod2 影响抗生素暴露后微生物的恢复力和结肠炎易感性。
Mucosal Immunol. 2019 May;12(3):720-732. doi: 10.1038/s41385-018-0128-y. Epub 2019 Jan 16.
7
Defining Dysbiosis in Inflammatory Bowel Disease.定义炎症性肠病中的菌群失调。
Immunity. 2019 Jan 15;50(1):8-10. doi: 10.1016/j.immuni.2018.12.028.
8
Mechanisms of Disease: Inflammatory Bowel Diseases.发病机制：炎症性肠病。
Mayo Clin Proc. 2019 Jan;94(1):155-165. doi: 10.1016/j.mayocp.2018.09.013.
9
FcαRI co-stimulation converts human intestinal CD103 dendritic cells into pro-inflammatory cells through glycolytic reprogramming.FcαRI共刺激通过糖酵解重编程将人肠道CD103树突状细胞转化为促炎细胞。
Nat Commun. 2018 Feb 28;9(1):863. doi: 10.1038/s41467-018-03318-5.
10
The Impact of NOD2 Variants on Fecal Microbiota in Crohn's Disease and Controls Without Gastrointestinal Disease.NOD2 变异对克罗恩病患者和无胃肠道疾病对照者粪便微生物群的影响。
Inflamm Bowel Dis. 2018 Feb 15;24(3):583-592. doi: 10.1093/ibd/izx061.