The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Defective IL10 Signaling Defining a Subgroup of Patients With Inflammatory Bowel Disease
Abstract
OBJECTIVES: Early onset inflammatory bowel diseases (EO-IBD) developing during the first year of life are likely to reflect inherited defects in key mechanism(s) controlling intestinal homeostasis, as recently suggested for interleukin 10 (IL10). Thus, we aimed to further elaborate the hypothesis of defective anti-inflammatory responses in patients with IBD. METHODS: The capacities of transforming growth factor β (TGFβ) and IL10 to inhibit proinflammatory cytokine production by monocyte-derived dendritic cells (MoDC) or peripheral blood cells (PBMC) was analyzed in 75 children with IBD, including 13 infants with EO-IBD (in whom autoimmune diseases or classical immunodeficiencies were ruled out). IL10 receptor-A/-B expression, STAT3 activation in response to IL6, IL10, IL21, IL22 were analyzed by FACS and western blotting. IL10RA and B genes were sequenced. The response to IL22 was tested in ileal/colonic tissue cultures. Tissue gene expression was analyzed by Taqman real-time polymerase chain reaction. RESULTS: Production of IL10 in response to bacterial motifs was normal in all IBD patients. In contrast to our original hypothesis, no defect of the anti-inflammatory potential of TGFβ and IL10 was observed in children with IBD or EO-IBD except two infants who presented with granuloma-positive colitis at 3 months of life: no response to IL10 was observed secondary to mutations in the α (p.R262C) or β (p.E141X) chain of IL10R, respectively, although a fully functional Jak-STAT3 pathway was present in both patients. When analyzing the regulation of intestinal bacterial clearance, we detected a defect in the patient with absent IL10 RB to upregulate protective transcripts in response to IL22, whereas all other EO-IBD patients, including the patient with an abnormal α chain, responded normally. CONCLUSIONS: Impaired IL10 signaling characterizes a subgroup of IBD patients, whereas the majority of children with severe IBD including EO forms normally produces and responds to IL10. Defective IL22 signaling may additionally impair intestinal epithelial clearance. Our data point out the complexity of IBD, which represent a group of distinct diseases with several pathogenetic abnormalities.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls
The Wellcome Trust Case Control Consortium, Management Committee, Burton, P. R., Clayton, D. G., Cardon, L. R., Craddock, N., Deloukas, P., Duncanson, A., Kwiatkowski, D. P., McCarthy, M. I., et al. (2007) · Nature · doi:10.1038/nature05911 · Cited by 9,442
Unravelling the pathogenesis of inflammatory bowel disease
Xavier, R. J., & Podolsky, D. K. (2007) · Nature · doi:10.1038/nature06005 · Cited by 4,364
Interleukin-10-deficient mice develop chronic enterocolitis
Kühn, R., Löhler, J., Rennick, D., Rajewsky, K., & Müller, W. (1993) · Cell · doi:10.1016/0092-8674(93)80068-p · Cited by 4,274
Abraham, C., & Cho, J. H. (2009) · New England Journal of Medicine · doi:10.1056/nejmra0804647 · Cited by 2,712
The Wellcome Trust Case Control Consortium, U.K.
Mossman, K. (2008) · Scientific American · doi:10.1038/scientificamerican0108-42a · Cited by 2,684
Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's disease
the NIDDK IBD Genetics Consortium, Barrett, J. C., the Belgian-French IBD Consortium, the Wellcome Trust Case Control Consortium, Hansoul, S., Nicolae, D. L., Cho, J. H., Duerr, R. H., Rioux, J. D., Brant, S. R., et al. (2008) · Nature Genetics · doi:10.1038/ng.175 · Cited by 2,593
Self-citationInterleukin-22 mediates early host defense against attaching and effacing bacterial pathogens
Zheng, Y., Valdez, P. A., Danilenko, D. M., Hu, Y., Sa, S. M., Gong, Q., Abbas, A. R., Modrusan, Z., Ghilardi, N., de Sauvage, F. J., et al. (2008) · Nature Medicine · doi:10.1038/nm1720 · Cited by 1,921
Inflammatory Bowel Disease and Mutations Affecting the Interleukin-10 Receptor
Glocker, E.-O., Kotlarz, D., Boztug, K., Gertz, E. M., Schäffer, A. A., Noyan, F., Perro, M., Diestelhorst, J., Allroth, A., Murugan, D., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0907206 · Cited by 1,461
Self-citationESPGHAN and ESPEN Guidelines Paediatric Parenteral Nutrition ‐ Annex: List of Products
(2005) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/01.mpg.0000181841.07090.f4 · Cited by 1,231
IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis
Sugimoto, K., Ogawa, A., Mizoguchi, E., Shimomura, Y., Andoh, A., Bhan, A. K., Blumberg, R. S., Xavier, R. J., & Mizoguchi, A. (2008) · Journal of Clinical Investigation · doi:10.1172/jci33194 · Cited by 1,023
Cited by
Anti-inflammatory effect of IL-10 mediated by metabolic reprogramming of macrophages
Ip, W. K. E., Hoshi, N., Shouval, D. S., Snapper, S., & Medzhitov, R. (2017) · Science · doi:10.1126/science.aal3535 · Cited by 1,375
Sun, M., Wu, W., Chen, L., Yang, W., Huang, X., Ma, C., Chen, F., Xiao, Y., Zhao, Y., Ma, C., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-05901-2 · Cited by 658
Pathophysiology of Inflammatory Bowel Disease: Innate Immune System
Saez, A., Herrero-Fernandez, B., Gomez-Bris, R., Sánchez-Martinez, H., & Gonzalez-Granado, J. M. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24021526 · Cited by 580
Gao, X., Cao, Q., Cheng, Y., Zhao, D., Wang, Z., Yang, H., Wu, Q., You, L., Wang, Y., Lin, Y., et al. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1720696115 · Cited by 400
Turner, D., Levine, A., Escher, J. C., Griffiths, A. M., Russell, R. K., Dignass, A., Dias, J. A., Bronsky, J., Braegger, C. P., Cucchiara, S., et al. (2012) · Journal of Pediatric Gastroenterology and Nutrition · doi:10.1097/mpg.0b013e3182662233 · Cited by 382
Self-citation
Metadata
- Authors
- Begue, B., Verdier, J., Rieux-Laucat, F., Goulet, O., Morali, A., Canioni, D., Hugot, J.-P., Daussy, C., Verkarre, V., Pigneur, B., Fischer, A., Klein, C., Cerf-Bensussan, N., & Ruemmele, F. M.
- Venue
- American Journal of Gastroenterology
- Published
- 2011-08
- Volume
- 106
- Issue
- 8
- Pages
- 1544-1555
- ISSN
- 0002-9270 (ISSN-L)
- OpenAlex
- W2059632816
- Cited by
- 262
- References
- 29
- FWCI
- 11.51
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Defective IL10 Signaling Defining a Subgroup of Patients With Inflammatory Bowel Disease. https://app.cochat.ai/papers/10.1038/ajg.2011.112
- The paper
- Begue, B., Verdier, J., Rieux-Laucat, F., Goulet, O., Morali, A., Canioni, D., Hugot, J.-P., Daussy, C., Verkarre, V., Pigneur, B., Fischer, A., Klein, C., Cerf-Bensussan, N., & Ruemmele, F. M. (2011). Defective IL10 Signaling Defining a Subgroup of Patients With Inflammatory Bowel Disease. American Journal of Gastroenterology. https://doi.org/10.1038/ajg.2011.112
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
