ArticleThe Journal of clinical investigation2021
NOD2 drives early IL-33-dependent expansion of group 2 innate lymphoid cells during Crohn's disease-like ileitis.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026Review
- Article
- Epithelial and stromal remodeling in murine Crohn's disease-like ileitis.bioRxiv : the preprint server for biology · 2025Article
- Review
- Intestinal IL-33 promotes microbiota-derived trimethylamine N -oxide synthesis and drives metabolic dysfunction-associated steatotic liver disease progression by exerting dual regulation on HIF-1α.Hepatology (Baltimore, Md.) · 2025Article
- The angiotensin receptor blocker, losartan, reduces inflammation and fibrosis, and prevents relapse of fibrosis after steroid-induced remission, in mice prone to Crohn's disease-like ileitis.Journal of Crohn's & colitis · 2025Article
- Review
- Host-pathobiont interactions in Crohn's disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- TMEM219 signaling promotes intestinal stem cell death and exacerbates colitis.The Journal of clinical investigation · 2025Article
- Immune-Modulating Effects of Low-Carbohydrate Ketogenic Foods in Healthy Canines.Current developments in nutrition · 2024Article
- Article
- The role of gut microbiota in intestinal disease: from an oxidative stress perspective.Frontiers in microbiology · 2024Review
- A Narrative Review of Cytokine Networks: Pathophysiological and Therapeutic Implications for Inflammatory Bowel Disease Pathogenesis.Biomedicines · 2023Review
- Microbial sensing in the intestine.Protein & cell · 2023Review
- Colitis-associated carcinogenesis: crosstalk between tumors, immune cells and gut microbiota.Cell & bioscience · 2023Review
- Microbiota-dependent regulation of costimulatory and coinhibitory pathways via innate immune sensors and implications for immunotherapy.Experimental & molecular medicine · 2023Review
- A Deep View of the Biological Property of Interleukin-33 and Its Dysfunction in the Gut.International journal of molecular sciences · 2023Review
- Intestinal Immune Imbalance is an Alarm in the Development of IBD.Mediators of inflammation · 2023Review
- Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Innate lymphoid cells (ILCs) are enriched at barrier surfaces, including the gastrointestinal tract. While most studies have focused on the balance between pathogenic group 1 ILCs (ILC1s) and protective ILC3s in maintaining gut homeostasis and during chronic intestinal inflammation, such as Crohn's disease (CD), less is known regarding ILC2s. Using an established murine model of CD-like ileitis, i.e., the SAMP1/YitFc (SAMP) mouse strain, we showed that ILC2s, compared with ILC1s and ILC3s, were increased within draining mesenteric lymph nodes and ilea of SAMP versus AKR (parental control) mice early, during the onset of disease. Gut-derived ILC2s from CD patients versus healthy controls were also increased and expanded, similarly to ILC1s, in greater proportion compared with ILC3s. Importantly, we report that the intracellular bacteria-sensing protein, nucleotide-binding oligomerization domaining-containing protein 2, encoded by Nod2, the first and strongest susceptibility gene identified for CD, promoted ILC2 expansion, which was dramatically reduced in SAMP mice lacking NOD2 and in SAMP mice raised under germ-free conditions. Furthermore, these effects occurred through a mechanism involving the IL-33/ST2 ligand-receptor pair. Collectively, our results indicate a functional link between NOD2 and ILC2s, regulated by the IL-33/ST2 axis, that mechanistically may contribute to early events leading to CD pathogenesis.
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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.