IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis.

By K. Sugimoto, A. Ogaẃa, E. Mizoguchi, Y. Shimomura, A. Andoh, A. Bhan, R. Blumberg, Ramnik J. Xavier, A. Mizoguchi. Journal of Clinical Investigation, 2008

1,078 citations recorded by the source corpus.

Subfields: Immunology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/dab5de5b3844df0bb95420f7bf4bce7264a66217

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. V. Kuchroo
2. H. Spits
3. D. Artis
4. R. Flavell
5. Markus F. Neurath
6. T. Korn
7. M. Oukka
8. N. Crellin

In Pathology and Forensic Medicine

1. H. Spits
2. M. V. D. van den Brink
3. T. Korn
4. F. Powrie
5. R. Flavell
6. E. Bettelli
7. M. Oukka
8. V. Kuchroo

Citations in the corpus

• Interleukins (from IL-1 to IL-38), interferons, transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases. (2016, background): “Although IL-22 has been associated with inflammatory disorders, it might also have anti-inflammatory effects.(96,97) For example, IL-22 inhibits IFN-g–induced secretion of the proinflammatory chemokines CCL5/RANTES and CXCL10/interferon-inducible protein 10 and antagonizes IFN-g in lung inflammation”
• Dendritic cells in intestinal immune regulation (2008, positive): “Furthermore, T H 17 cells themselves may also contribute to the healing process in the intestine through the production of IL-22 (Ref”
• Interleukin-22: immunobiology and pathology (2015, background): “However, in later periods after IL-22 has been induced, levels of IL-22BP can increase indicating a regulatory role after the initial early effects of IL-22 (217, 220, 221).”
• Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease (2008, background): “has already shown that IL-22 holds promise for IBD therapy (Sugimoto et al., 2008).”
• Cytokine signaling modules in inflammatory responses. (2008, background): “…technically challenging model of ulcerative colitis, IL-22 administration via pressurized local microinjection of IL-22-expressing vectors was shown to have a robust anti-inflammatory effect in the intestine mediated in part via Stat3 activation in colonic epithelial cells (Sugimoto et al., 2008).”
• STAT3 links IL-22 signaling in intestinal epithelial cells to mucosal wound healing (2009, background): “Accordingly, IL-22 gene delivery was shown to ameliorate DSS-induced colitis (Sugimoto et al., 2008).”
• Anti- and Pro-inflammatory Roles of TGF-β, IL-10, and IL-22 In Immunity and Autoimmunity (2009, background): “be protective in acute inflammatory models, such as hepatitis, as well as during chronic inflammation such as inflammatory bowel disease [46 ,52,61].”