ArticleNature communications2021
NOD2 deficiency increases retrograde transport of secretory IgA complexes in Crohn's disease.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- Oil-Coated Nanoplastics Induce Rapid Membrane Disruption and Severe Intestinal Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oral-Gut Microbiome Axis in Crohn's Disease: A Potential Role of Ectopic Colonization.Microorganisms · 2026Review
- Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.Journal of gastroenterology · 2025Review
- Gut expression of CD71 and co-localisation with Dec-1 associated with high levels of serum SIgA and disease activity in SpA.Scientific reports · 2025Article
- Advancements in the Extraction, Characterization, and Bioactive Potential of Laminaran: A Review.Foods (Basel, Switzerland) · 2025Review
- Autophagy in inflammatory bowel disease: immunization, etiology, and therapeutic potential.Frontiers in immunology · 2025Review
- Selective IgA Deficiency and Aseptic Liver Abscess as Initial Indicators of Crohn's Disease in a Young Woman: A Case Study.The American journal of case reports · 2024Article
- NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis.Cell death & disease · 2024Article
- Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Intestinal Mucosal Immune Barrier: A Powerful Firewall Against Severe Acute Pancreatitis-Associated Acute Lung Injury via the Gut-Lung Axis.Journal of inflammation research · 2024Review
- Identification of antigen-presentation related B cells as a key player in Crohn's disease using single-cell dissecting, hdWGCNA, and deep learning.Clinical and experimental medicine · 2023Article
- Microbial sensing in the intestine.Protein & cell · 2023Review
- The Underappreciated Role of Secretory IgA in IBD.Inflammatory bowel diseases · 2023Article
- Multi-omics in Crohn's disease: New insights from inside.Computational and structural biotechnology journal · 2023Review
- Intestinal fungi and antifungal secretory immunoglobulin A in Crohn's disease.Frontiers in immunology · 2023Review
- Exosomes derived from dental pulp stem cells accelerate cutaneous wound healing by enhancing angiogenesis via the Cdc42/p38 MAPK pathway.International journal of molecular medicine · 2022Article
- Impact of Dextran-Sodium-Sulfate-Induced Enteritis on Murine Cytomegalovirus Reactivation.Viruses · 2022Article
- Alteration of microbiota antibody-mediated immune selection contributes to dysbiosis in inflammatory bowel diseases.EMBO molecular medicine · 2022Article
- Host gene effects on gut microbiota in type 1 diabetes.Biochemical Society transactions · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.