title: Alterations in NK cell phenotype in relation to liver steatosis in children with chronic hepatitis C.
abstract: NK cells were found to play an important role in liver fibrosis, a process commonly seen in a chronic liver disease such as chronic hepatitis C (CHC). The aim of this study was to evaluate potential differences in relation to coexisting liver steatosis in children with chronic hepatitis C. The study group consisted of 31 children with chronic hepatitis, aged 7-18 years (mean = 15 ± 2 years). Blood samples were taken prior to liver biopsy. The METAVIR scale was used for histological evaluation. Peripheral lymphocytes were subjected to monoclonal antibodies to CD56 antigen, KIRs and NKG2D antigens. Cells were assayed by flow cytometry for the ratio of positive cells and mean fluorescence intensity (MFI). Results were evaluated regarding the presence of liver steatosis. Significantly higher mean AST activity as well as higher AST-to-platelets ratio index (APRI) was observed in a group of children with coexisting liver steatosis. These children had significantly higher MFI for CD158e and lower MFI for NKG2D. All CHC patients had significantly higher MFI for NKG2D than the controls. The proportion of cells with expression of CD158i, KIR2D and APRI was found independent predictors of liver steatosis in univariate analysis and body mass index in logistic regression. The expression of NK cell receptors is altered in coexisting steatosis that may influence long-term prognosis in CHC.
authors.affiliation: Department of Infectious Diseases and Child Neurology, University of Medical Sciences, ul. Szpitalna 27/33, 60-572, Poznań, Poland, mania@mp.pl.
authors.forename: Anna
authors.initials: A
authors.lastname: Mania
authors.forename: Mariusz
authors.initials: M
authors.lastname: Kaczmarek
authors.forename: Paweł
authors.initials: P
authors.lastname: Kemnitz
authors.forename: Iwona
authors.initials: I
authors.lastname: Mozer-Lisewska
authors.forename: Jan
authors.initials: J
authors.lastname: Sikora
authors.forename: Magdalena
authors.initials: M
authors.lastname: Figlerowicz
authors.forename: Aldona
authors.initials: A
authors.lastname: Woźniak
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Mazur-Melewska
authors.forename: Wojciech
authors.initials: W
authors.lastname: Służewski
authors.forename: Jan
authors.initials: J
authors.lastname: Żeromski
mesh_terms: D000293:Adolescent; D019002:CD56 Antigen / Q000276:immunology / Q000378:metabolism; D002648:Child; D005234:Fatty Liver / Q000276:immunology*; D005260:Female; D019698:Hepatitis C, Chronic / Q000276:immunology*; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D008103:Liver Cirrhosis / Q000276:immunology; D008297:Male; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000276:immunology / Q000378:metabolism*; D054340:Receptors, KIR / Q000276:immunology / Q000378:metabolism*; D054341:Receptors, KIR3DL1 / Q000378:metabolism
chemical_list: D019002:CD56 Antigen; C527085:KLRK1 protein, human; D055655:NK Cell Lectin-Like Receptor Subfamily K; D054340:Receptors, KIR; D054341:Receptors, KIR3DL1
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