Analysis of CD137 function in patients with inflammatory bowel disease

Doctoral Researcher

Associated Doctoral Researcher

Background and current state of research

In 2020, doctoral researchers from at least two or more RTG projects working in different disciplines could apply for extra funding for a small interdiciplinary project within the RTG.

The aim of this offer is

  • to enhance the scientific collaboration within the RTG,
  • to widen interdisciplinary skills of the doctoral researchers and
  • to provide the doctoral researchers the opportunity to practice
    • writing a proposal,
    • working as a team,
    • coordinating a small own research project (one of the junior researchers helds the position of the project leader).

Four proposals have been submitted and reviewed by two external reviewers and two members of the supervisory board. The results were pretty clear, all of the proposals received good scores. However, there were two first places and two second places. Both 1st and 2nd winners were close from the score. Therefore, the overall funding budget was devided between the four groups giving all of them the chance to make this experience.

Under the header "Our goals" you find more information about this mini-proposal.

 

Our goals

Inflammatory bowel diseases (IBD) are intestinal disorders that cause prolonged inflammation of the digestive tract. The two major forms are Crohn’s disease (CD) and ulcerative colitis (UC). It is known that several members of the tumor necrosis factor (TNF) receptor family are involved in the inflammation of the gut tissues.
One important regulator and member of the TNF receptor family is CD137, which is expressed on activated T lymphocytes. High levels of soluble CD137 can be detected in sera of patients with autoimmune diseases like rheumatoid arthritis. It is supposed that the soluble form of CD137 is generated by differential splicing. According to the literature, it could also be released by shedding through a metalloprotease. Indeed, several members of the TNF receptor family are released by the most prominent members of the disintegrin-like metalloproteases (ADAMs) family, ADAM10 and ADAM17. Prelimary experiments of our lab indicate that this might also hold true for CD137.
In this study we want to find out if there are differences in the level of soluble CD137 in blood samples of IBD patients compared to the control, whether there might be a differences in the release and if there are important microbial antigens which induce a strong regulatory T cell (Treg) response and CD137 shedding in IBD.

Project leader: Jana Seidel

Project budget: 15.000 €

Running time: April - December 2020