The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
IL-22 Induces Lipopolysaccharide-Binding Protein in Hepatocytes: A Potential Systemic Role of IL-22 in Crohn’s Disease
Abstract
Crohn′s disease (CD) is a common, chronic, inflammatory bowel disease characterized by intestinal infiltration of activated immune cells and distortion of the intestinal architecture. In this study, we demonstrate that IL-22, a cytokine that is mainly produced by activated Th1 and Th17 cells, was present in high quantities in the blood of CD patients in contrast to IFN-γ and IL-17. In a mouse colitis model, IL-22 mRNA expression was elevated predominantly in the inflamed intestine but also in the mesenteric lymph nodes. IL-22BP, the soluble receptor for IL-22, demonstrated an affinity to IL-22 that was at least 4-fold higher than its membrane-bound receptor, and its strong constitutive expression in the intestine and lymph nodes was decreased in the inflamed intestine. To investigate the possible role of systemic IL-22 in CD, we then administered IL-22 to healthy mice and found an up-regulation of LPS-binding protein (LBP) blood levels reaching concentrations known to neutralize LPS. This systemic up-regulation was associated with increased hepatic but not renal or pulmonary LBP mRNA levels. IL-22 also enhanced the secretion of LBP in human primary hepatocytes and HepG2 hepatoma cells in vitro. This increase was mainly transcriptionally regulated and synergistic with that of other LBP inducers. Finally, elevated LBP levels were detected in CD patients and the mouse colitis model. These data suggest that systemic IL-22 may contribute to the prevention of systemic inflammation provoked by LPS present in the blood of CD patients through its induction of hepatic LBP.
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Citations
Cites
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
Cua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
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
Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
Zheng, Y., Danilenko, D. M., Valdez, P., Kasman, I., Eastham-Anderson, J., Wu, J., & Ouyang, W. (2007) · Nature · doi:10.1038/nature05505 · Cited by 1,862
Increased expression of interleukin 17 in inflammatory bowel disease
Fujino, S., Andoh, A., Bamba, S., Ogawa, A., Hata, K., Araki, Y., Bamba, T., & Fujiyama, Y. (2003) · Gut · doi:10.1136/gut.52.1.65 · Cited by 1,713
Structure and Function of Lipopolysaccharide Binding Protein
Schumann, R. R., Leong, S. R., Flaggs, G. W., Gray, P. W., Wright, S. D., Mathison, J. C., Tobias, P. S., & Ulevitch, R. J. (1990) · Science · doi:10.1126/science.2402637 · Cited by 1,672
Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
Murphy, C. A., Langrish, C. L., Chen, Y., Blumenschein, W., McClanahan, T., Kastelein, R. A., Sedgwick, J. D., & Cua, D. J. (2003) · The Journal of Experimental Medicine · doi:10.1084/jem.20030896 · Cited by 1,669
IL-23 is essential for T cell–mediated colitis and promotes inflammation via IL-17 and IL-6
Yen, D., Cheung, J., Scheerens, H., Poulet, F., McClanahan, T., Mckenzie, B., Kleinschek, M. A., Owyang, A., Mattson, J., Blumenschein, W., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci21404 · Cited by 1,542
IL-22 Increases the Innate Immunity of Tissues
Wolk, K., Kunz, S., Witte, E., Friedrich, M., Asadullah, K., & Sabat, R. (2004) · Immunity · doi:10.1016/j.immuni.2004.07.007 · Cited by 1,359
Self-citationWolk, K., Witte, E., Wallace, E., Döcke, W., Kunz, S., Asadullah, K., Volk, H., Sterry, W., & Sabat, R. (2006) · European Journal of Immunology · doi:10.1002/eji.200535503 · Cited by 922
Self-citation
Cited by
Korn, T., Bettelli, E., Oukka, M., & Kuchroo, V. K. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132710 · Cited by 4,873
Regulation and Functions of the IL-10 Family of Cytokines in Inflammation and Disease
Ouyang, W., Rutz, S., Crellin, N. K., Valdez, P. A., & Hymowitz, S. G. (2011) · Annual Review of Immunology · doi:10.1146/annurev-immunol-031210-101312 · Cited by 1,925
Sonnenberg, G. F., Fouser, L. A., & Artis, D. (2011) · Nature Immunology · doi:10.1038/ni.2025 · Cited by 1,044
The genetics and immunopathogenesis of inflammatory bowel disease
Cho, J. H. (2008) · Nature Reviews Immunology · doi:10.1038/nri2340 · Cited by 940
Interleukin-22: Immunobiology and Pathology
Dudakov, J. A., Hanash, A. M., & van den Brink, M. R. M. (2015) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032414-112123 · Cited by 905
Metadata
- Authors
- Wolk, K., Witte, E., Hoffmann, U., Doecke, W.-D., Endesfelder, S., Asadullah, K., Sterry, W., Volk, H.-D., Wittig, B. M., & Sabat, R.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-05-01
- Volume
- 178
- Issue
- 9
- Pages
- 5973-5981
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1508191015
- Cited by
- 270
- References
- 46
- FWCI
- 11.55
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: IL-22 Induces Lipopolysaccharide-Binding Protein in Hepatocytes: A Potential Systemic Role of IL-22 in Crohn’s Disease. https://app.cochat.ai/papers/10.4049/jimmunol.178.9.5973
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- Wolk, K., Witte, E., Hoffmann, U., Doecke, W.-D., Endesfelder, S., Asadullah, K., Sterry, W., Volk, H.-D., Wittig, B. M., & Sabat, R. (2007). IL-22 Induces Lipopolysaccharide-Binding Protein in Hepatocytes: A Potential Systemic Role of IL-22 in Crohn’s Disease. The Journal of Immunology. https://doi.org/10.4049/jimmunol.178.9.5973
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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.
