The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Role of the novel Th17 cytokine IL-17F in inflammatory bowel disease (IBD): Upregulated colonic IL-17F expression in active Crohnʼs disease and analysis of the IL17F p.His161Arg polymorphism in IBD
Abstract
BACKGROUND: Interleukin (IL)-17F, produced in IL-23R-expressing Th17 cells, is a novel member of the IL-17 cytokine family. Given the association of IL23R with inflammatory bowel disease (IBD), we characterized the role of IL-17F in IBD including its intestinal gene expression and the effect of the IL17F p.His161Arg polymorphism on disease susceptibility and phenotype of Crohn's disease (CD) and ulcerative colitis (UC). In addition, we analyzed the IL17F p.His161Arg polymorphism for potential epistasis with IL23R and NOD2/CARD15 variants. METHODS: Intestinal IL-17F mRNA expression was measured by quantitative polymerase chain reaction (PCR). Genomic DNA from 1682 individuals (CD: n = 499; UC: n = 216; controls: n = 967) was analyzed for the presence of the IL17F p.His161Arg polymorphism, the 3 NOD2 variants, p.Arg702Trp, p.Gly908Arg, and p.Leu1007fsX1008, and 10 CD-associated IL23R variants. RESULTS: Intestinal IL-17F mRNA expression was 4.4-fold increased in inflamed colonic lesions compared to uninflamed biopsies in CD (P = 0.016) but not in UC. However, the mean intestinal IL-17F mRNA expression was higher in UC than in CD (P < 0.0001). The IL17F p.His161Arg substitution was observed with similar frequencies in IBD patients and controls and was not associated with a certain disease phenotype, but weakly associated with a low body mass index (BMI; P = 0.009) and an earlier age of disease onset (P = 0.039) in UC. There was no evidence for epistasis between the IL17F p.His161Arg polymorphism and IBD-associated single nucleotide polymorphisms within the IL23R gene. CONCLUSIONS: Intestinal IL17F gene expression is increased in active CD. The IL17F p.His161Arg polymorphism is not associated with IBD susceptibility and has no epistatic interaction with CD-associated IL23R variants.
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
Unravelling the pathogenesis of inflammatory bowel disease
Xavier, R. J., & Podolsky, D. K. (2007) · Nature · doi:10.1038/nature06005 · Cited by 4,364
Veldhoen, M., Hocking, R. J., Atkins, C. J., Locksley, R. M., & Stockinger, B. (2006) · Immunity · doi:10.1016/j.immuni.2006.01.001 · Cited by 3,605
Silverberg, M. S., Satsangi, J., Ahmad, T., Arnott, I. D., Bernstein, C. N., Brant, S. R., Caprilli, R., Colombel, J.-F., Gasche, C., Geboes, K., et al. (2005) · Canadian Journal of Gastroenterology · doi:10.1155/2005/269076 · Cited by 3,409
A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene
Duerr, R. H., Taylor, K. D., Brant, S. R., Rioux, J. D., Silverberg, M. S., Daly, M. J., Steinhart, A. H., Abraham, C., Regueiro, M., Griffiths, A., et al. (2006) · Science · doi:10.1126/science.1135245 · Cited by 3,039
Liang, S. C., Tan, X.-Y., Luxenberg, D. P., Karim, R., Dunussi-Joannopoulos, K., Collins, M., & Fouser, L. A. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20061308 · Cited by 2,330
Zhou, L., Ivanov, I. I., Spolski, R., Min, R., Shenderov, K., Egawa, T., Levy, D. E., Leonard, W. J., & Littman, D. R. (2007) · Nature Immunology · doi:10.1038/ni1488 · Cited by 2,141
Development, cytokine profile and function of human interleukin 17-producing helper T cells
Wilson, N. J., Boniface, K., Chan, J. R., McKenzie, B. S., Blumenschein, W. M., Mattson, J. D., Basham, B., Smith, K., Chen, T., Morel, F., et al. (2007) · Nature Immunology · doi:10.1038/ni1497 · Cited by 2,035
Classification of Inflammatory Bowel Disease
Lennard-Jones, J. E. (1989) · Scandinavian Journal of Gastroenterology · doi:10.3109/00365528909091339 · Cited by 2,011
Reciprocal T H 17 and Regulatory T Cell Differentiation Mediated by Retinoic Acid
Mucida, D., Park, Y., Kim, G., Turovskaya, O., Scott, I., Kronenberg, M., & Cheroutre, H. (2007) · Science · doi:10.1126/science.1145697 · Cited by 1,982
Hampe, J., Franke, A., Rosenstiel, P., Till, A., Teuber, M., Huse, K., Albrecht, M., Mayr, G., De La Vega, F. M., Briggs, J., et al. (2007) · Nature Genetics · doi:10.1038/ng1954 · Cited by 1,897
Cited by
Western Diet and the Immune System: An Inflammatory Connection
Christ, A., Lauterbach, M., & Latz, E. (2019) · Immunity · doi:10.1016/j.immuni.2019.09.020 · Cited by 907
Brand, S. (2009) · Gut · doi:10.1136/gut.2008.163667 · Cited by 668
Self-citationLeppkes, M., Becker, C., Ivanov, I. I., Hirth, S., Wirtz, S., Neufert, C., Pouly, S., Murphy, A. J., Valenzuela, D. M., Yancopoulos, G. D., et al. (2009) · Gastroenterology · doi:10.1053/j.gastro.2008.10.018 · Cited by 444
Differential regulation of interleukin 17 and interferon production in inflammatory bowel disease
Rovedatti, L., Kudo, T., Biancheri, P., Sarra, M., Knowles, C. H., Rampton, D. S., Corazza, G. R., Monteleone, G., Di Sabatino, A., & MacDonald, T. T. (2009) · Gut · doi:10.1136/gut.2009.182170 · Cited by 338
Catechins and Their Therapeutic Benefits to Inflammatory Bowel Disease
Fan, F.-Y., Sang, L.-X., & Jiang, M. (2017) · Molecules · doi:10.3390/molecules22030484 · Cited by 336
Metadata
- Authors
- Seiderer, J., Elben, I., Diegelmann, J., Glas, J., Stallhofer, J., Tillack, C., Pfennig, S., Jürgens, M., Schmechel, S., Konrad, A., Göke, B., Ochsenkühn, T., Müller-Myhsok, B., Lohse, P., & Brand, S.
- Venue
- Inflammatory Bowel Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-04
- Volume
- 14
- Issue
- 4
- Pages
- 437-445
- ISSN
- 1078-0998 (ISSN-L)
- OpenAlex
- W2097087846
- Cited by
- 329
- References
- 55
- FWCI
- 10.55
- 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: Role of the novel Th17 cytokine IL-17F in inflammatory bowel disease (IBD): Upregulated colonic IL-17F expression in active Crohnʼs disease and analysis of the IL17F p.His161Arg polymorphism in IBD. https://app.cochat.ai/papers/10.1002/ibd.20339
- The paper
- Seiderer, J., Elben, I., Diegelmann, J., Glas, J., Stallhofer, J., Tillack, C., Pfennig, S., Jürgens, M., Schmechel, S., Konrad, A., Göke, B., Ochsenkühn, T., Müller-Myhsok, B., Lohse, P., & Brand, S. (2008). Role of the novel Th17 cytokine IL-17F in inflammatory bowel disease (IBD): Upregulated colonic IL-17F expression in active Crohnʼs disease and analysis of the IL17F p.His161Arg polymorphism in IBD. Inflammatory Bowel Diseases. https://doi.org/10.1002/ibd.20339
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.
