Scientists uncover new therapeutic target for treating colorectal tumors TUS_PR CellReports
It turns out that innate immune receptors, particularly those expressed in the gut, such as C-type lectin receptors , are responsible for the development of IBD. However, CLRs also play a vital role in the regulation of gut microbiota and defense against pathogens. As a result, a balance needs to be struck to maintain intestinal homeostasis.
Dendritic cell immunoreceptor is one such CLR that is responsible for maintaining homeostasis of the immune and skeletal systems. Previous studies have suggested that DCIR negatively regulates both innate and acquired immune responses. Blocking DCIR could, therefore, potentially boost immunity against colonAgainst this backdrop, a research group led by Professor Yoichiro Iwakura of Tokyo University of Science in Japan has now shed light on this issue.
To their surprise, they found that the mice lacking DCIR showed reduced colitis severity and AOM-DSS–induced colorectal tumor growth. Moreover, compared to the wild-type mice , the DCIR-deficient mice showed lower body weight loss as well as reduced proinflammatory cell infiltration in the colon. What do these observations imply? Prof. Iwakura explains,"Our findings point to the fact that intestinal carcinogenesis and inflammation are facilitated by DCIR signaling, which points to the possibility that blocking DCIR might preventCorroborating this possibility, the study further revealed that the use of an antibody called"anti-NA2" against asialo-biantennary-N-glycans , a ligand to DCIR, reduced DSS colitis symptoms and prevented colorectal tumor growth.
The researchers are excited by these findings. Speaking about the practical applications of their study, Prof. Iwakura says,"Our results suggest that therapeutics targeting DCIR and its ligands could be used to effectively treatThis study could open doors to novel therapeutic strategies for treating colorectal tumors, improving not only the lives of patients with IBD but also the understanding of the pathogenesis of human diseases.
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