Multiple immune cells and their products in the liver together form a complex and unique immune microenvironment, and preclinical models have demonstrated the importance of imbalances in the hepatic immune microenvironment in liver inflammatory diseases and immunocompromised liver diseases. Various immunotherapies have been attempted to modulate the hepatic immune microenvironment for the purpose of treating liver diseases. Mesenchymal stem cells (MSCs) have a comprehensive and plastic immunomodulatory capacity. On the one hand, they have been tried for the treatment of inflammatory liver diseases because of their excellent immunosuppressive capacity; On the other hand, MSCs have immune-enhancing properties in immunocompromised settings and can be modified into cellular carriers for targeted transport of immune enhancers by genetic modification, physical and chemical loading, and thus they are also used in the treatment of immunocompromised liver diseases such as chronic viral infections and hepatocellular carcinoma. In this review, we discuss the immunological basis and recent strategies of MSCs for the treatment of the aforementioned liver diseases. Specifically, we update the immune microenvironment of the liver and summarize the distinct mechanisms of immune microenvironment imbalance in inflammatory diseases and immunocompromised liver diseases, and how MSCs can fully exploit their immunotherapeutic role in liver diseases with both immune imbalance patterns.
Background: Kidney injury of systemic lupus erythematosus (SLE) contributes to major mortality of SLE. To explore biomarkers is necessary for diagnosing and supervising SLE-associated kidney injury. However, few effective biomarkers can be used for it.Methods: Apriori algorithm of association rules was employed to identify laboratory biomarkers related to SLE-associated kidney injury. Logistic regression analysis was conducted to identify its risk factors, and spearman correlation analysis was used to evaluate the correlation between biomarkers and disease activity of SLE-associated kidney injury.Results: Ten biomarkers were mined by association rule mining. Among them, triglycerides, lactate dehydrogenase and α-hydroxybutyrate dehydrogenase were significantly higher, and haemoglobin and haematocrit were significantly lower in patients with SLE-associated kidney injury than in those without kidney injury. Furthermore, triglycerides were an independent risk factor for SLE-associated kidney injury. There were more patients with SLE-associated kidney injury, SLE disease activity index 2000, blood urea nitrogen, creatinine, proteinuria and urine pathology cast (P-CAST) in the high-triglyceride group. Triglycerides were positively correlated with proteinuria and P-CAST, and they were negatively correlated with albumin and immunoglobulin G. The area under the receiver operating characteristic curve for triglycerides was 0.72,and the optimal cut-off level was 1.84 mmol/l, which provided 64.4% sensitivity and 75.9% specificity in predicting SLE-associated kidney dysfunction. 50% SLE-associated kidney injuries patients with negative proteinuria could be identified by high triglyceride levels. In addition, higher levels of triglycerides were found at the time of onset of kidney injury. With the change in SLE-associated kidney injury, the variation in triglyceride levels is opposite to the evaluated glomerular filtration rate.Conclusion: triglycerides are associated with SLE-associated kidney injury and may be a potential biomarker for auxiliary diagnosis of SLE-associated kidney injury.
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