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Hepatitis B virus causes mixed cryoglobulinaemia by driving clonal expansion of innate B-cells producing a VH1-69-encoded antibody


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12

 

  1. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy. marcella.visentini@uniroma1.it
  2. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  3. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  4. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  5. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  6. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  7. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  8. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  9. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  10. Division of Gastroenterology and Hepatology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  11. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
  12. Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.

CER8559
2016 Vol.34, N°3 ,Suppl.97
PI 0028, PF 0032
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PMID: 26811981 [PubMed]

Received: 23/04/2015
Accepted : 20/07/2015
In Press: 20/01/2016
Published: 27/05/2016

Abstract

OBJECTIVES:
To investigate the expression of a VH1-69-encoded idiotype, and the phenotypic and functional features of monoclonal B-cells from patients with type II mixed cryoglobulinaemia (MC) secondary to chronic hepatitis B virus (HBV) infection.
METHODS:
B-cell immunophenotype and expression of a VH1-69-encoded idiotype were investigated by flow cytometry. B-cell proliferative responses to stimuli were investigated by the CFSE dilution assay.
RESULTS:
Two out of five patients with chronic HBV studied had massive monoclonal expansion of VH1-69-expressing B-cells. These cells had the peculiar CD21low phenotype and low responsiveness to stimuli typical of the VH1-69-expressing B-cells commonly expanded in MC secondary to hepatitis C virus (HCV) infection. In both patients, anti-HBV therapy led to the regression of MC and of VH1-69+ B-cell expansion.
CONCLUSIONS:
VH1-69-encoded antibodies are known to preferentially recognise a variety of viral proteins including HCV E2, influenza A virus haemagglutinin and HIV gp41/gp120, and may serve as innate first line antiviral defense. Thus, like HCV, HBV may cause MC by protracted antigenic stimulation of VH1-69-expressing B-cells.

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