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Compromised function of natural killer cells in acute and chronic viral hepatitis
Sebastian Lunemann1,2,
David F. G. Malone2,
Julia Hengst1,2,
Kerstin Port1,
Jan Grabowski1,
Katja Deterding1,
Antoaneta Markova1,
Birgit Bremer1,
Verena Schlaphoff1,
Markus Cornberg1,
Michael P. Manns1,
Johan K. Sandberg2,
Hans-Gustaf Ljunggren2,
Niklas K. Björkström2,3 and
Heiner Wedemeyer1
+ Author Affiliations
1Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, 30161 Hannover , Germany
2Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, S-14186 Stockholm, Sweden
3Liver Immunology Laboratory, Department of Medicine, Karolinska Institutet, S-14186 Stockholm, Sweden
Contact Information corresponding author: Heiner Wedemeyer, Medizinische Hochschule Hannover, Klinik für Gastroenterologie, Hepatologie und Endokrinologie, Carl-Neuberg-Str. 1, 30625 Hannover, Germany, Telefon: +49 511 532 6814, Telefax: +49 511 532 8662, [email protected]
Abstract
Background. Natural killer (NK) cells are an integral part of the innate immune system. They have been suggested to play an important role in both defense against viral hepatitis and the pathogenesis of other liver diseases.
Methods. NK cells from 134 individuals including patients with acute hepatitis B and C as well as chronic hepatitis B, C, and delta (D) patients were studied.
Results. Infection with viral hepatitis was associated with increased frequencies of NK cells in the peripheral blood; that NK cells showed a less activated phenotype and were compromised in cytolotytic function and cytokine production in all viral hepatitis infections: Hepatitis virus infections did not alter NK cell differentiation and the activity and severity of liver disease were reflected by alterations of NK cell surface receptors as demonstrated by principal component analysis.
Conclusion. NK cell phenotypic and functional alterations can equally be observed in HBV, HCV, and HDV infections. Instead, patterns of NK cell alterations differ in acute and chronic infections. Thus, our data suggest a common mechanism in the alteration of NK cell phenotype and function with unique variations that depend on disease activity rather than virus-specific factors.
Received May 27, 2013.
Revision received August 9, 2013.
Accepted September 6, 2013.
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