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CD47 is an immunoglobulin that is overexpressed on the surface of a variety of cancer cells. CD47 forms a signaling complex with signal regulatory protein alpha (SIRPα), prompting the escape of cancer cells from macrophage-mediated phagocytosis. In recent years, CD47 has been shown to be highly expressed in many types of solid tumors and is associated with poor prognosis in patients. More and more studies have shown that inhibition of the CD47-SIRPα signaling pathway can promote adaptive immune responses and enhance the phagocytosis of tumor cells by macrophages. Humanized anti-CD47 IgG4 monoclonal antibody has been studied in clinical trials for the treatment of a variety of advanced solid tumors and lymphomas, demonstrating a sound safety profile and achieving partial remission in some patients. In this review we discuss the structure and function of CD47 and the mechanism of CD47 regulation in tumors, summarize the research progress in therapeutic antibody drugs targeting CD47 and a bottleneck in research that targeted drugs are more prone to result in serious adverse effects, and evaluated the potential of the applying CD47-SIRPα signaling pathway in anti-cancer therapy., (Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).)

Background: Hepatorenal and hepatopulmonary syndrome are common clinical diseases; however, their mechanisms have not been fully elucidated. Our aim was to determine whether liver injury by bile duct ligation (BDL) causes modifications in kidney and lung tissue in mice, and to explore the possible mechanism of these changes., Methods: BDL in mice was used as a research model. Pathologic changes of liver, kidney, and lung tissue were observed by hematoxylin-eosin (H&E) staining. The expression of IGFBPrP1, NF-κB, TNF-α, and IL-6 were investigated in liver, kidney, and lung tissue by immunohistochemical staining and western blot. The correlation between IGFBPrP1 and NF-κB, TNF-α, and IL-6 protein expression in liver, kidney, and lung tissues of each group was analyzed by the Pearson method., Results: H&E staining showed, after BDL administration in mice, different degrees of inflammatory change in liver, kidney, and lung tissues of mice in each group. The results of immunohistochemical staining and western blot analysis showed increased expressions of IGFBPrP1, NF-κB, TNF-α, and IL-6 after BDL. Pearson correlation analysis showed that IGFBPrP1 positively correlated with the expressions of NF-κB, TNF-α, and IL-6., Conclusion: Liver injury caused by bile duct ligation can lead to kidney and lung tissue injury in mice. The mechanism of injury may be related to the high expression of liver injury factor IGFBPrP1, transcription factor NF-κB, proinflammatory cytokine TNF-α, and IL-6 in kidney and lung tissue. Moreover, an increased expression level of IGFBPrP1 may be accompanied by the activation of the NF-κB inflammatory pathway., Competing Interests: None., (IJCEP Copyright © 2020.)