Too much of a specific oncogene in chronic intestinal cause inflammation. These genes play not only in cancer a role.
CED – Chronic inflammatory bowel diseases such as ulcerative colitis or Crohn’s disease based on mistakes the body’s own immune system. The result are often in pain, thrust-like complaints such as stomach and cramps or diarrhea. The exact causes are, in spite of strong efforts of the research remains unknown.
Oncogene as the culprit unmasked
Scientists at the Helmholtz centre in Munich and the Johannes Gutenberg University in Mainz have now uncovered a new mechanism*. He is a part of the puzzle in the pathogenesis of CED. The researchers found that the well-known oncogene Bcl-3 is increased in the gut of Colitis patients. The culprit is also involved in various types of cancer. As it turned out, it brings too much of the Oncogene, the immune system out of balance: There are blocked processes, thanks to which the T-cells of the immune system remain passive. The T-cells called the immune cells that normally prevent excessive reactions of the immune system. Thus, a tolerance to your own body. Due to the Blockade regulate the T-cells, the immune system is no longer – as a result, the inflammation processes. The oncogene is actually one of the triggers to the CED.
The results of the Mainz and Munich-based researchers contribute significantly to a better understanding of chronic intestinal inflammation . Because now it is clear that and how the oncogene causes the inflammation in the intestine. On the basis of the new attack in the long term points for causal therapies. So the scientists are now looking for drugs that the Blockade of the T-cells stop.
New approaches to the treatment of IBD are desperately needed. Because of this the intestine can not be cured disease: A therapy, which eliminates the causes. What has now been found on the oncogene Bcl-3, can patients hope.
*Reissig, S. et al. Bcl-3 Inhibits NF-kB Gene Activity in Regulatory T cells and Modulates their Suppressive Capacity. Nature Communications, 2017