DGIM awards the Theodor-Frerichs Prize to SFB 841 Scientist Prof. Samuel Huber

5 May 2017

With ascending trend, approximately 400,000 people in Germany suffer from Crohn’s disease and ulcerative colitis. In both diseases the peaceful coexistence of bacteria, building the intestinal flora, and the immune system is disturbed. Scientists around the group of Prof. Dr. Samuel Huber were able to identify a fundamental molecular mechanism, which contributes to disruption of healing process of patients’ intestinal mucosa and the development of a chronic disease. Their work published in Science has now been awarded with the prestigious Theodor-Frerichs-Prize 2017 by the German Society of Internal Medicine (DGIM).

Preisverleihung_Theodor-Frerichs-Preis_Huber_DGIM 2017
Bestoval of the Theodor Frerichs Prize 2017 to Prof. Samuel Huber (center); Photo: DGIM / Sebastian Dark

“I am very happy about this award. I would like to thank my group for the excellent work and thanks to our close collaborator Prof. Dr. Nicola Gagliani, I. Department of Medicine & General, Visceral and Thoracic Surgery Department, both departments of the UKE, and Prof. Dr. Richard Flavell, Yale University, USA”, Prof. Huber states. He is research group leader at the I. Department of Medicine of the UKE and project manager in the SFB 841.

Chronic inflammatory diseases (CED) are not yet curable. They are accompanied by a significant reduction of life quality for patients. A targeted therapy is missing, also because it is not yet clear, which specific signalling pathways trigger and maintain the inflammatory activities in the intestinal mucosa. The scientists took a huge step forward in the investigation of possible causes. “We were able to demonstrate that there is a misregulation of the so-called IL-22-IL-22BP axis in CED patients. Interleukin 22 (IL-22) is essential for the healing of the attacked mucous membranes. This messenger substance cannot fulfil its role because its antagonist, the interleukin 22 binding protein (IL-22BP), is produced abundantly already at the very beginning of the inflammation of CD4 + T cells. As a consequence, IL-22 is bound and disabled. The wound healing cannot be initiated and the disease becomes chronic”, Huber says.

The starting point for efficient therapy in chronic inflammatory diseases therefore could be to specifically target the IL-22BP. “Previous treatment options for CED suppress nonspecific inflammatory activities, which do have serious side effects, such as an increased risk of infection. Our results suggest that substances directly blocking the binding protein positively affect the course of the disease”, Prof. Huber explains. In addition, the scientists suggest that the IL-22-IL-22BP axis misregulation plays an important role, not exclusively in CED patients. The new findings could significantly advance the investigation of other inflammatory and autoimmune diseases.

More Information about the subproject C8 “IL-22 and IL-22BP in regeneration of liver and liver carcinogenesis” you will find here.

Literature:

Pelczar P, Witkowski M, Perez LG, Kempski J, Hammel AG, Brockmann L, Kleinschmidt D, Wende S, Haueis C, Bedke T, Witkowski M, Krasemann S, Steurer S, Booth CJ, Busch P, König A, Rauch U, Benten D, Izbicki JR, Rösch T, Lohse AW, Strowig T, Gagliani N, Flavell RA, Huber S

A pathogenic role for T cell-derived IL-22BP in inflammatory bowel disease
Science 2016; 354(6310): 358-362.

In a short video interview Prof. Huber explains the importance of the excellent awarded research work: