Role of Tim-3 in hepatitis B virus infection:An overview  

作　　者：yuan liu li-fen gao xiao-hong liang chun-hong ma 

机构地区：[1]Department of Immunology,Key Laboratory for Experimental,Teratology of Ministry of Education,Shandong Provincial Key Laboratory of Infection and Immunology,Shandong University School of Medicine,Jinan 250012,Shandong province,China

出　　处：《World Journal of Gastroenterology》2016年第7期2294-2303,共10页世界胃肠病学杂志（英文版）

基　　金：the National Natural Science Fund for Out-standing Youth Fund,No.81425012;National Nature Science Foundation of China,No.81100203,No.81371831 and No.91129704;Research Fund for the Doctoral Program of Higher Education of China(RFDP),No.20110131110034

摘　　要：Hepatitis B virus(HBV) infection has received increasing public attention. h BV is the prototypical member of hepadnaviruses, which naturally infect only humans and great apes and induce the acute and persistent chronic infection of hepatocytes. A large body of evidence has demonstrated that dysfunction of the host anti-viral immune response is responsible for persistent HBV replication, unresolved inflammation and disease progression. Many regulatory factors are involved in immune dysfunction. Among these, T cell immunoglobulin domain and mucin domain-3(Tim-3), one of the immune checkpoint proteins, has attracted increasing attention due to its critical role in regulating both adaptive and innate immune cells. In chronic HBV infection, Tim-3 expression is elevated in many types of immune cells, such as T helper cells, cytotoxic T lymphocytes, dendritic cells, macrophages and natural killer cells. Tim-3 over-expression is often accompanied by impaired function of the abovementioned immunocytes, and Tim-3 inhibition can at least partially rescue impaired immune function and thus promote viral clearance. A better understanding of the regulatory role of Tim-3 in host immunity during HBV infection will shed new light on the mechanisms of h BV-related liver disease and suggest new therapeutic methods for intervention.Hepatitis B virus(HBV) infection has received increasing public attention. h BV is the prototypical member of hepadnaviruses, which naturally infect only humans and great apes and induce the acute and persistent chronic infection of hepatocytes. A large body of evidence has demonstrated that dysfunction of the host anti-viral immune response is responsible for persistent HBV replication, unresolved inflammation and disease progression. Many regulatory factors are involved in immune dysfunction. Among these, T cell immunoglobulin domain and mucin domain-3(Tim-3), one of the immune checkpoint proteins, has attracted increasing attention due to its critical role in regulating both adaptive and innate immune cells. In chronic HBV infection, Tim-3 expression is elevated in many types of immune cells, such as T helper cells, cytotoxic T lymphocytes, dendritic cells, macrophages and natural killer cells. Tim-3 over-expression is often accompanied by impaired function of the abovementioned immunocytes, and Tim-3 inhibition can at least partially rescue impaired immune function and thus promote viral clearance. A better understanding of the regulatory role of Tim-3 in host immunity during HBV infection will shed new light on the mechanisms of h BV-related liver disease and suggest new therapeutic methods for intervention.

关 键 词：TIM-3 HEPATITIS B VIRUS INFLAMMATION IMMUNITY LIVER disease 

分 类 号：R512.62[医药卫生—内科学]