title: Liver-infiltrating CD56 positive T lymphocytes in hepatitis C virus infection.
abstract: OBJECTIVE
  Hepatitis C virus (HCV) is a major cause of post-transfusional and sporadic hepatitis, and leads to chronic liver disease. It has been suggested that virus-specific cytotoxic T lymphocytes are responsible for liver injuries that occur in HCV-infected patients. However, the detailed characteristics of these lymphocytes have not yet been defined. We have previously reported that CD56+ T lymphocytes, as intermediates between natural killer cell and T lymphocytes, predominantly infiltrated the liver and were increased in patients with chronic hepatitis related to HCV (CH-C).
  
  
  METHODS
  We obtained peripheral blood and liver tissues from 32 patients diagnosed as having CH-C, and 10 other liver disease patients (5 chronic hepatitis related to HBV, 5 alcoholics), and analyzed peripheral blood and liver-infiltrating lymphocytes using flow cytometric and immunohistochemical techniques.
  
  
  RESULTS
  The CD56+ T lymphocyte ratio in the liver of patients with a high histology activity index (HAI) score for chronic hepatitis was higher than that of patients with a low HAI score and patients with other liver diseases. In addition, T lymphocytes from patients with chronic hepatitis with a high HAI score carried mostly gamma delta-TCR. There was a correlation between the ratio of CH-C and serum alanine aminotransferase, category I (periportal inflammation and necrosis), and IV (fibrosis) of the HAI scoring system. The ratio was highest in zone 1 of the hepatic lobules.
  
  
  CONCLUSIONS
  The correlation between CD56+ T lymphocyte ratios and hepatocellular damage was examined. These findings suggest strongly that liver-infiltrating CD56+ T lymphocytes play an important pathologic role in hepatocellular injury in CH-C.
authors.affiliation: Department of Internal Medicine III, Niigata University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yonekura
authors.forename: T
authors.initials: T
authors.lastname: Ichida
authors.forename: K
authors.initials: K
authors.lastname: Sato
authors.forename: S
authors.initials: S
authors.lastname: Yamagiwa
authors.forename: M
authors.initials: M
authors.lastname: Uchida
authors.forename: S
authors.initials: S
authors.lastname: Sugahara
authors.forename: S
authors.initials: S
authors.lastname: Ito
authors.forename: T
authors.initials: T
authors.lastname: Abo
authors.forename: H
authors.initials: H
authors.lastname: Asakura
mesh_terms: D000328:Adult; D000368:Aged; D000410:Alanine Transaminase / Q000097:blood; D000911:Antibodies, Monoclonal / Q000276:immunology; D017252:CD3 Complex / Q000032:analysis; D019002:CD56 Antigen / Q000032:analysis* / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D005260:Female; D005434:Flow Cytometry; D016174:Hepacivirus / Q000276:immunology / Q000502:physiology; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology* / Q000473:pathology / Q000821:virology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000276:immunology / Q000473:pathology / Q000821:virology; D016131:Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011948:Receptors, Antigen, T-Cell / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D017252:CD3 Complex; D019002:CD56 Antigen; D011948:Receptors, Antigen, T-Cell; D007770:L-Lactate Dehydrogenase; D000410:Alanine Transaminase