ArticleGastroenterology2015
SAMP1/YitFc mice develop ileitis via loss of CCL21 and defects in dendritic cell migration.
Article in Gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- A multidimensional platform to support intestinal epithelial and immune cell co-culture.Frontiers in nutrition · 2026Article
- Epithelial and stromal remodeling in murine Crohn's disease-like ileitis.bioRxiv : the preprint server for biology · 2025Article
- Lymphatic alterations in Crohn's disease: the villain or victim.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Landscape of Interactions between Stromal and Myeloid Cells in Ileal Crohn's Disease; Indications of an Important Role for Fibroblast-Derived CCL-2.Biomedicines · 2024Article
- Crohn's disease as the intestinal manifestation of pan-lymphatic dysfunction: An exploratory proposal based on basic and clinical data.World journal of gastroenterology · 2024Review
- The role of dendritic cells in tertiary lymphoid structures: implications in cancer and autoimmune diseases.Frontiers in immunology · 2024Review
- Knowledge mapping and research trends of IL-33 from 2004 to 2022: a bibliometric analysis.Frontiers in immunology · 2023Article
- Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease.International journal of molecular sciences · 2022Review
- Aging impairs arterial compliance via Klotho-mediated downregulation of B-cell population and IgG levels.Cellular and molecular life sciences : CMLS · 2022Article
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- Sex-based differences in inflammatory bowel diseases: a review.Therapeutic advances in gastroenterology · 2020Review
- IL-33 and IL-18 in Inflammatory Bowel Disease Etiology and Microbial Interactions.Frontiers in immunology · 2019Review
- Uncovering Pathogenic Mechanisms of Inflammatory Bowel Disease Using Mouse Models of Crohn's Disease-Like Ileitis: What is the Right Model?Cellular and molecular gastroenterology and hepatology · 2017Review
- Lymphoid Aggregates Remodel Lymphatic Collecting Vessels that Serve Mesenteric Lymph Nodes in Crohn Disease.The American journal of pathology · 2016Article
- Mechanisms of Microbe-Host Interaction in Crohn's Disease: Dysbiosis vs. Pathobiont Selection.Frontiers in immunology · 2015Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe lymphatic chemokine CCL21 is required for dendritic cell (DC) migration from tissues to lymph nodes, which helps establish tolerance to foreign yet harmless antigens. We demonstrate that CCL21 is almost completely absent from SAMP1/YitFc (SAMP) mice, which spontaneously develop chronic ileitis that resembles Crohn's disease, and that DC migration is severely impaired in these mice compared with AKR mice (controls). Toll-like receptor agonists like the Toll-like receptor 7 agonist R848 induce DC maturation and mobilization.
methodsWe collected intestinal and other tissues and mesenteric lymph nodes (MLN) from SAMP mice. Expression of CCL21 was measured by quantitative reverse transcription polymerase chain reaction and immunofluorescence analyses; spontaneous and induced migration of DCs were assessed by flow cytometry. We analyzed production of retinoic acid by DCs and their ability to induce development of regulatory T cells. Mice were fed R848 to determine its effects on migration of DCs and development of ileitis in SAMP mice.
resultsSAMP mice expressed almost no CCL21 in any tissue tested. Their CD11b(+)CD103(+) DCs were defective in migration from the ileal lamina propria to the MLN. DCs from SAMP mice also had a greatly reduced ability to produce retinoic acid and induce development of regulatory T cells compared with control mice. Young SAMP mice had reduced CCL21 expression and decreased DC migration before developing ileitis. Administration of R848 to adult SAMP mice increased migration of DC to the MLN and development of regulatory T cells there, and reduced the severity of ileitis.
conclusionsLoss of CCL21 signaling and DC migration is required for development of ileitis in SAMP mice. Reagents such as R848, which activate DC migration to the MLN, may be developed as treatments for patients with Crohn's disease.
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Registered trials
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.