The body's immune system is at risk of developing chronic intestinal disorders. Researchers have found that excessive amounts of oncogene Bcl-3 is the cause for these diseases.
The research found that chronic intestinal disorders such as ulcerative colitis and crohn's disease are caused by the body's own immune defense system. Sufferers frequently experience episodic symptoms such as abdominal pain, cramps, and diarrhea. Researchers are still trying to identify the precise underlying origins of these problems.
"With the help of our cooperation partners, we were able to demonstrate that the level of the Bcl-3 protein, which also plays a role in the development of various cancerous diseases, is elevated in the intestinal tract of colitis patients and is indeed a trigger of the disease," said Dr. Nadine Hovelmeyer, head of the work group at the Mainz-based Institute for Molecular Medicine.
"We were able to demonstrate that Bcl-3 suppresses the activation of Tregs by preventing the necessary genes from being read. Bcl-3 interacts with the transcription factor p50, which is otherwise responsible for activation, and blocks it," shared Dr. Elke Glasmacher, head of the team at the Institute for Diabetes and Obesity in Munich.
Dr. Sonja Reissig, lead author of the publication and research associate at Mainz University Medical Center noted, "Consequentially, the regulatory T-cells remain passive, the immune system is no longer regulated, and inflammatory processes begin to take place. Experiments using various models have revealed that elevated quantities of Bcl-3 cause certain cells to migrate to the intestines, where they trigger a severe inflammatory response."
Dr. Hovelmeyer concluded by saying, "The results represent a major contribution towards our understanding of chronic intestinal inflammation and hopefully over the long-term will help us discover aspects that we can target with new therapies."
While, her colleague Professor Ari Waisman, Director of the Institute for Molecular Medicine at the Mainz University Medical Center stated, "We are currently focusing on the search for new active agents that will prevent the interaction between Bcl-3 and p50, thus maintaining normal Treg functionality."
The study was published in Journal Nature Communications.