Dendritic cells that stimulate T-cell attack on cancer tumors Inflammatory bowel disease (IBD) is a disease name that encompasses Crohn’s disease and ulcerative colitis, which are chronic inflammation of the gastrointestinal tract.
Prolonged inflammation of the gastrointestinal tract increases the risk of colorectal cancer (colon cancer).
Therefore, understanding the mechanism of IBD is important for preventing colorectal cancer.
It is known that innate immune receptors such as ‘type C lectin receptors’ (CLRs), which appear frequently in the intestine, are deeply involved in the development of IBD.
However, CLRs also play an important role in the regulation of the gut microbiota and blocking pathogens.
Therefore, to maintain ‘intestinal homeostasis’, CLRs must work in a balanced way.
The ‘dendritic cell immune receptor’ (DCIR), which is involved in maintaining homeostasis of the immune system and the skeletal system, is also a kind of ‘C-type lectin receptor’.
DCIR has so far been known to suppress both innate and adaptive immune responses.
This means that DCIR expression must be blocked to enhance the immune response against inflammatory bowel disease.
However, research results have shown that DCIR signals can directly promote the development of colorectal cancer and intestinal inflammation.
This discovery could be of great help in the development of new colorectal cancer treatments and improving the quality of life of patients with inflammatory bowel disease.
The results of this research conducted by Professor Yoichiro Iwakura’s team at the Institute of Biomedical Sciences, Tokyo University of Science (TUS), Japan, were published online in the international journal ‘Cell Reports’ on the 2nd (local time). published as a thesis.
Effects of DCIR Signal SuppressionIn the mammalian immune system, dendritic cells mainly function to deliver antigens.
It mediates the innate immune response and the acquired immune response by presenting pathogenic substances on its surface and notifying other immune cells.
Professor Iwakuro’s team tested how enteritis and colon tumors develop in a mouse model without DCIR.
First, it was important to induce colon tumors similar to those found in patients with inflammatory bowel disease.
So, sodium dextran sulfate (DSS, an enteritis-causing substance) and azoxymethane (AOM, a neurotoxic chemical) were mixed with water and fed to the mice.
However, the result was completely unexpected.
In mice without DCIR, the growth of enteritis and colon tumors was suppressed.
These mice also had less intestinal tissue infiltration of pro-inflammatory cells and lost less body weight than the control group.
Professor Iwakura said, “This suggests that the DCIR signal promotes the development of colon cancer and inflammation. Blocking the DCIR signal may prevent ulcerative colitis and colorectal cancer.”
The research team also presented agonists and targets that can be applied in practice.
The use of an NA2 (diatomic sodium) inhibitory antibody against asialo-biantennary-N-glycans, a DCIR ligand (ligand binding molecule), alleviates the growth of DSS-induced enteritis and colorectal cancer. .
This suggests that the development of therapeutic agents targeting DCIR and related ligands can be effective in autoimmune diseases, inflammatory bowel diseases, and colorectal cancer.
Professor Iwakura’s team expects that the results of this study will lead to the development of effective treatments.
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