Scientists have found a new way to treat colorectal tumors
According to a recent study, mice lacking the dendritic cell immunoreceptor are resistant to colitis and the development of colon tumors.
The term “inflammatory bowel disease” (IBD) refers to Crohn’s disease and ulcerative colitis, two conditions marked by persistent inflammation of the gastrointestinal tract.
The occurrence of colorectal tumors is frequently a result of this condition. Therefore, reducing the incidence of colonic tumors requires an understanding of the pathogenesis of IBD.
It turns out that the onset of IBD is caused by innate immune receptors, particularly those expressed in the gut, such as C-type lectin receptors (CLRs).
CLRs are essential for controlling the gut microbiota and defending against pathogens, as well. Therefore, a delicate balance must be achieved to preserve intestinal homeostasis.
One such CLR that is in charge of preserving the immune and skeletal systems’ homeostasis is the dendritic cell immunoreceptor (DCIR).
According to earlier research, DCIR appears to negatively control both innate and acquired immune responses. Therefore, blocking DCIR might enhance immunity against colon tumors. Its function in intestinal immunity, however, is still unknown.
In light of this, researchers from the Tokyo University of Science (TUS), Japan, have now clarified this problem. The group’s investigation, which was just published in Cell Reports, looked at the growth of colon tumors and colitis in DCIR-deficient mouse models.
In order to accomplish this, the team fed the mice drinking water containing azoxymethane (AOM), a neurotoxic chemical, and dextran sodium sulphate (DSS), a synthetic sulphated polysaccharide, in order to induce colon tumors similar to those seen in people with IBD.
They were shocked to discover that the mice lacking DCIR had less severe colitis and less colorectal tumor growth brought on by AOM-DSS.
Additionally, the DCIR-deficient mice displayed less body weight loss and less proinflammatory cell infiltration in the colon when compared to the wild-type mice (control).
According to Professor Yoichiro Iwakura, the research’s principal investigator, “Our results indicate that intestinal carcinogenesis and inflammation are promoted by DCIR signalling, suggesting that blocking DCIR might prevent ulcerative colitis and colon cancer.”
The study also found that the use of an antibody called “anti-NA2” against asialo-biantennary-N-glycans (NA2), a ligand (binding molecule) to DCIR, decreased DSS colitis symptoms and stopped the growth of colorectal tumors, supporting this theory.
Our findings suggest that therapeutics targeting DCIR and its ligands could be used to successfully treat cancer, IBD, and autoimmune diseases, which have historically been challenging to treat, said Iwakura.