Literature DB >> 23558709

Alterations in NK cell phenotype in relation to liver steatosis in children with chronic hepatitis C.

Anna Mania1, Mariusz Kaczmarek, Paweł Kemnitz, Iwona Mozer-Lisewska, Jan Sikora, Magdalena Figlerowicz, Aldona Woźniak, Katarzyna Mazur-Melewska, Wojciech Służewski, Jan Żeromski.   

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.

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Year:  2013        PMID: 23558709      PMCID: PMC3781300          DOI: 10.1007/s10753-013-9632-0

Source DB:  PubMed          Journal:  Inflammation        ISSN: 0360-3997            Impact factor:   4.092


  18 in total

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Authors:  Michael Kremer; Ian Neil Hines; Richard Jameson Milton; Michael Daryl Wheeler
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3.  Natural killer inhibitory receptor expression associated with treatment failure and interleukin-28B genotype in patients with chronic hepatitis C.

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Journal:  Hepatology       Date:  2011-08-24       Impact factor: 17.425

4.  Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA.

Authors:  S Bauer; V Groh; J Wu; A Steinle; J H Phillips; L L Lanier; T Spies
Journal:  Science       Date:  1999-07-30       Impact factor: 47.728

5.  Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity.

Authors:  L E Adinolfi; M Gambardella; A Andreana; M F Tripodi ; R Utili; G Ruggiero
Journal:  Hepatology       Date:  2001-06       Impact factor: 17.425

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7.  Transforming growth factor beta 1 inhibits expression of NKp30 and NKG2D receptors: consequences for the NK-mediated killing of dendritic cells.

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Journal:  Proc Natl Acad Sci U S A       Date:  2003-03-19       Impact factor: 11.205

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10.  IL28B, HLA-C, and KIR variants additively predict response to therapy in chronic hepatitis C virus infection in a European Cohort: a cross-sectional study.

Authors:  Vijayaprakash Suppiah; Silvana Gaudieri; Nicola J Armstrong; Kate S O'Connor; Thomas Berg; Martin Weltman; Maria Lorena Abate; Ulrich Spengler; Margaret Bassendine; Gregory J Dore; William L Irving; Elizabeth Powell; Margaret Hellard; Stephen Riordan; Gail Matthews; David Sheridan; Jacob Nattermann; Antonina Smedile; Tobias Müller; Emma Hammond; David Dunn; Francesco Negro; Pierre-Yves Bochud; Simon Mallal; Golo Ahlenstiel; Graeme J Stewart; Jacob George; David R Booth
Journal:  PLoS Med       Date:  2011-09-13       Impact factor: 11.069

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  2 in total

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Authors:  Q Zheng; Y Y Zhu; J Chen; Y B Ye; J Y Li; Y R Liu; M L Hu; Y C Zheng; J J Jiang
Journal:  Clin Exp Immunol       Date:  2015-04-12       Impact factor: 4.330

2.  CD4+ and CD8+ T Cell Activation in Children with Hepatitis C.

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Journal:  J Pediatr       Date:  2015-12-30       Impact factor: 4.406

  2 in total

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