title: Expression of CD39 on FoxP3+ T regulatory cells correlates with progression of HBV infection.
abstract: BACKGROUND
  Although it is known that regulatory T cells (Tregs) can suppress the function of effector T cells, and may contribute to impaired immune response, the precise role of Tregs during the course of hepatitis B virus (HBV) infection remains to be elucidated. A newly identified subset of the CD4+Foxp3+ Tregs, the CD39+ Tregs, has been associated with viral infections and autoimmune diseases. Therefore, we hypothesized that this discrete Treg subset may contribute to the chronic infection of HBV.
  
  
  RESULTS
  Initial characterization studies of healthy peripheral CD39+FoxP3+CD4+ T cells revealed that the majority were CD45RA- Treg cells. Subsequent analysis of HBV-infected patients (38 asymptomatic HBV carriers (AsCs), 37 chronic active hepatitis B (CAH), 29 HBV-associated acute-on-chronic liver failure (ACLF)) and healthy individuals (25 controls) was conducted to assess association with HBV copy number and the liver injury marker alanine aminotransferase (ALT). A higher percentage of CD39+ Tregs was detected within the population of FoxP3+CD4+ T cells in peripheral blood of AsCs patients. Moreover, the percentage of CD39+ Tregs was significantly less in CAH and ACLF patients. The increased proportions of circulating CD39+ Tregs were positively correlated with serum viral load, but inversely correlated with serum ALT level.
  
  
  CONCLUSIONS
  These findings not only suggest that CD39+ Treg cells may be involved in HBV disease progression but also identify CD39+ Tregs as a dynamic immune regulatory cell population that may represent a new target of immunomodulatory therapeutic interventions.
authors.affiliation: Institute of Immunology, PLA, Third Military Medical University, Chongqing 400038, People Republic of China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Tang
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Zheng
authors.forename: Bing
authors.initials: B
authors.lastname: Ni
authors.forename: Yuzhang
authors.initials: Y
authors.lastname: Wu
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000276:immunology*; D001081:Apyrase / Q000276:immunology*; D058070:Asymptomatic Diseases; D015704:CD4 Antigens / Q000378:metabolism; D018791:CD4 Lymphocyte Count; D018450:Disease Progression; D005260:Female; D051858:Forkhead Transcription Factors / Q000276:immunology; D006515:Hepatitis B virus / Q000276:immunology*; D019694:Hepatitis B, Chronic / Q000150:complications / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D017114:Liver Failure, Acute / Q000209:etiology / Q000276:immunology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D019562:Viral Load; D055815:Young Adult
chemical_list: D015703:Antigens, CD; D015704:CD4 Antigens; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; D001081:Apyrase; C067869:CD39 antigen