Science publication: Dysregulation of IL-22-IL-22BP-axis in IBD
21 October 2016
Ulcerative Colitis and Crohn’s disease are increasingly common inflammatory bowel diseases (IBD). Since IBD is characterized by chronic inflammation, most of its therapies nowadays are being directed against these inflammatory responses, but cannot or do not directly promote mucosal healing. Relapsing flares and opportunistic infections that often occur as a consequence of the immune suppression are the resulting problems. Thus one major goal in the field of chronic inflammation, especially in IBD, is to identify the exact mechanisms that link inflammation and barrier dysfunction.
CRC scientists Prof. Dr. Samuel Huber & Prof. Dr. Nicola Gagliani and their colleagues have now made a significant progress in this regard. Prof. Huber explains: “We were able to show that a dysregulation of the IL-22-IL-22BP-axis is involved in the development of IBD. The function of Interleukin 22 (IL-22) is to promote healing of damaged intestinal mucosa. However, interleukin 22 binding protein (IL-22BP), the soluble antagonist of IL-22, is over expressed by CD4+ T cells in the intestine of IBD patients. Thus IL-22 cannot exert its tissue protective function.”
Furthermore, it is suggested that a dysregulation of the IL-22-IL-22BP-axis does not only play an important role in IBD but also in other chronic diseases. “The question why diseases become chronic is an important research issue of the CRC 841. These new findings will make a decisive impact on research into inflammation and autoimmune diseases,” says Prof. Dr. Ansgar W. Lohse, spokesperson of the CRC 841. Within CRC 841, Prof. Huber’s project focusses on the role of IL-22 and IL-22BP in liver regeneration and carcinogenesis.
For more information on Prof. Huber’s project C8: IL-22 and IL-22BP in liver regeneration and carcinogenesis
Read the complete press information: UKE scientists identify one cause of inflammatory bowel disease
Penelope Pelczar, Mario Wittkowski, Laura Garcia Perez et al., A pathogenic role for T-cell derived IL-22BP in inflammatory bowel disease.