CD73,also known as Ecto-5'-nucleotidase(eNT),is a multifunctional transmembrane glycoprotein with a molecular weight of 70 kD,which is anchored to the cell membrane by glycosyl phosphatidylinositol(GPI),exists in various cells of human body and plays different biological functions in various diseases.Studies have found that CD73 can cooperate with CD39 to complete the adenosine signaling pathway,ATP and ADP can catalyze AMP to generate adenosine in CD39,and then CD73 can catalyze AMP to generate adenosine.In recent years,more and more studies have focused on the role of CD73 in digestive diseases.This review aims to elucidate the biological role of CD73,analyze the research progress of immune regulation mechanism of CD73 in gastrointestinal dis-eases from the aspects of inflammation and tumor,and point out the importance of CD73 in the treatment and prognosis of intestinal diseases.

CD73,also known as Ecto-5'-nucleotidase(eNT),is a multifunctional transmembrane glycoprotein with a molecular weight of 70 kD,which is anchored to the cell membrane by glycosyl phosphatidylinositol(GPI),exists in various cells of human body and plays different biological functions in various diseases.Studies have found that CD73 can cooperate with CD39 to complete the adenosine signaling pathway,ATP and ADP can catalyze AMP to generate adenosine in CD39,and then CD73 can catalyze AMP to generate adenosine.In recent years,more and more studies have focused on the role of CD73 in digestive diseases.This review aims to elucidate the biological role of CD73,analyze the research progress of immune regulation mechanism of CD73 in gastrointestinal dis-eases from the aspects of inflammation and tumor,and point out the importance of CD73 in the treatment and prognosis of intestinal diseases.

Abstract: Objective This study aimed to investigate the expression of CD73 in colonic tissues in Crohn's disease (CD) and its significance and possible mechanism of action. Methods Thirty male BALB/c mice were randomly divided into normal control group, model group and intervention group. The control group was fed normally, and the model group was treated with TNBS+40% alcohol enema to establish a mouse model of Crohn's disease induced by chronic inflammation. The intervention group was treated with AB-680 intraperitoneally on the second day of each enema based on the model group. Mice body weight, fecal traits and fecal occult blood were recorded for disease activity index (DAI) score of inflammatory bowel disease. The animals were sacrificed at 7th week, their colonic tissues were removed, weighed and measured. The tissue inflammation was observed by standard hematoxylin-eosin (HE) staining. Masson staining was used to measure the area of collagen in colon tissue of mice. CD73 was detected by fluorescence quantitative PCR and immunohistochemistry. The expression levels of TGF-β, TNF-α and IL-6 in colon tissue of mice were determined by ELISA. Results The DAI score was (0.10±0.16) in the control group, (2.80±0.79) in the model group, and (3.07±0.34) in the intervention group. Compared with the control group, the DAI scores of the model and intervention groups were increased significantly (P<0.05). Compared with the model group, the DAI score of the intervention group was significantly increased (P<0.05). HE staining showed that there was no inflammation in the colon of the control group, while the colon of the model group and the intervention group showed typical inflammatory manifestations such as edema and congestion, inflammatory cell infiltration, and mucosal ulcer. The area ratio of collagen in the control group was (4.95±0.82)%, in the model group was (24.62±1.46)%, and in the intervention group was (54.47±2.75)%. Compared with the control group, the area ratio of collagen in the model group and the intervention group was significantly increased (P<0.05). Compared with the model group, the area ratio of collagen in the intervention group was significantly increased (P<0.05). Compared with the control group, the expression of CD73 in colon tissue of the model group and the intervention group was significantly increased (P<0.05). Compared with the model group, the expression of CD73 in colon tissue of the intervention group was decreased (P<0.05). Compared with the control group, the expressions of TGF-β, TNF-α and IL-6 in the model group and the intervention group were significantly increased (P<0.05). Compared with the model group, the expression of TGF-β, TNF-α and IL-6 in the intervention group decreased (P<0.05). Conclusions CD73 is upregulated in colon tissue of CD mice, it can inhibit inflammatory reaction and improve fibrosis by up-regulating TGF-β expression. On the other hand, CD73 can aggravate the inflammatory response in CD intestinal inflammation and fibrosis by up-regulating the expression of IL-6 and TNF-α. Therefore, CD73 may play a bidirectional regulatory role in intestinal inflammation and fibrosis of CD.