Objective To study the effect of CpG containing oligodeoxynucleotide(CpG-ODN) on the phenotypes,function and expression of signal transductors and activators of transcription(STAT) and suppressors of cell signaling(SOCS) of peripheral blood dendritic cells(DC) in patients with chronic hepatitis B(CHB).Methods Monocytes isolated from peripheral blood of CHB and healthy volunteers were cultured and induced by granulocyte-monocyte colony stimulating factor(GM-CSF) and interleukin-4(IL-4).Then,CpG-ODN or TNF-? were added to stimulate the immatured DC,their effects on the phenotypes and function of DC were evaluated.(The expression of) signaling molecules of STAT1,3,4,5,6 and SOCS1,3 in DC were detected by Western blotting.Results The(expression) rates of HLA-DR of DC in CHB with the treatment of CpG-ODN or TNF-? were obviously increased;Both the IL-12p70 expression and stimulating capacity of DC to allogenic T lymphocytes were improved significantly in CpG-ODN group and TNF-? group(P

Esophageal variceal bleeding is a severe complication of cirrhotic portal hypertension and the main cause of mortality in patients. Studies revealed no significant differences in emergency hemostasis rate,fatality rate,and rebleeding rate between patients receiving endo-scopic treatment and vasoactive agents.The advances in emergency management of esophageal variceal bleeding,including endoscopic band ligation,sclerotherapy,and use of vasoactive agents,are reviewed,with emphasis on emergency endoscopic treatment and drug therapy for esophageal variceal bleeding.

As a series of multifunctional cells,recent studies indicate that most of the CD4 + T lymphocyte subsets involve in the tumor angiogenesis and invasion,the apoptosis of tumor cells,and the expressions of acute phase proteins and cancer-promoting genes by activating or inhibiting the innate immune cells,the adaptive immune cells and non-immune cells,thus function as tumor promoters or inhibitors in hepatocellular carcinoma (HCC).

Autoimmune hepatitis is a type of autoimmune disease and has known pathogenesis at present, which is believed to be associated with immune imbalance in the body. In inflammatory diseases, regulatory B cells (Bregs) inhibits the differentiation of CD4+ T lymphocytes into T helper 1 cells and T helper 17 cells by secreting interleukin-10 (IL-10) to inhibit inflammatory response. Patients with autoimmune hepatitis have reductions in the level of IL-10 in peripheral blood and the number and function of Bregs, which leads to the fact that Bregs cannot effectively inhibit inflammatory response, suggesting that Bregs play a certain role in the pathogenesis of autoimmune hepatitis. This article reviews the mechanism of action of Breg subsets in autoimmune hepatitis.

Serum cholinesterase (ChE) is synthesized by hepatic parenchymal cells and is released into blood immediately after synthesis,and therefore,serum ChE can be used as an objective and sensitive indicator of liver function.Serum ChE has been used as an independent factor for the evaluation of liver function for a long time and can reflect the synthetic function of the liver and help to determine the severity of liver diseases.Combined measurement of serum ChE and serum prealbumin,total cholesterol,total bile acid,and prothrombin time has an important value in the diagnosis and treatment of liver diseases.At the same time,serum ChE combined with Child-Turcotte-Pugh score or MELD score can accurately evaluate liver reserve function,which may help with the prognostic evaluation of patients with liver diseases.

Immunoglobulin G4-related sclerosing cholangitis (IgG4-SC) is a new type of secondary sclerosing cholangitis which was discovered recently and has unknown pathogenesis.IgG4-SC is characterized by an increased serum level of immunoglobulin G4 (IgG4),chronic progressive obstructive jaundice,diffuse or local infiltration of a large number of IgG4-positive plasma cells and lymphocytes,fibrosis,and obstructive phlebitis.This article reviews the diagnosis and treatment of IgG4-SC and its association with primary sclerosing cholangitis and cholangiocarcinoma.

Nonalcoholic fatty liver disease (NAFLD) is closely associated with insulin resistance and genetic susceptibility and is one of the chronic liver diseases that threaten human health .Under certain conditions, Th17 cells and regulatory T (Treg) cells can be transformed to each other to maintain immune homeostasis.In recent years, more and more studies have been performed on the involvement of Th 17 and Treg cells in the development and progression of liver diseases .Th17 cells, Treg cells, and their balance may become the new targets for the treatment of NAFLD.This article reviews the latest research advances in the association of Th 17 and Treg cells with NAFLD and the role of Th17/Treg balance in the development and progression of NAFLD .

Autoimmune hepatitis (AIH) is a chronic autoimmune disease in the liver, with major clinical manifestations of positive autoantibody, abnormal elevation of aminotransferases, and hypergammaglobulinemia. Current studies have shown that regulatory T (Treg)/T helper 17 (Th17) and T helper 1 (Th1)/T helper 2 (Th2) imbalance is one of the mechanisms of the development and progression of AIH. OX40 (also known as CD134, TNFRSF4, or ACT35) and its ligand OX40L are members of the tumor necrosis factor family, and they participate in immune response as co-stimulators of T cell activation and can regulate Treg/Th17 and Th1/Th2 balance, thus affecting the progression of various autoimmune diseases. However, there are few reports on the role of OX40 and OX40L in AIH. With reference to related articles, this article reviews the role of Treg/Th17 and Th1/Th2 balance in AIH and the potential association between OX40/OX40L (new targets for immunological diagnosis and treatment) and AIH.

Nonalcoholic fatty liver disease is a group of diseases with unclear pathophysiological mechanism and is closely associated with metabolic syndrome. Bacterial components and metabolites produced by gut microbiota can regulate glucose and lipid metabolism, inflammatory response, and oxidative stress, and bile acids regulate immune function, energy metabolism, and material metabolism through various signaling pathways after activating their receptors. Gut microbiota and bile acids interact with each other through enterohepatic circulation, and the changes of their structure and function are involved in the development and progression of nonalcoholic fatty liver disease. This article reviews the effect of the homeostatic dysregulation of gut microbiota and bile acids and their interactions on nonalcoholic fatty liver disease.