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Hepatitis B virus causes mixed cryoglobulinaemia by driving clonal expansion of innate B-cells producing a VH1-69-encoded antibody
M. Visentini1, S. Pascolini2, M. Mitrevski3, R. Marrapodi4, M. Del Padre5, L. Todi6, A. Camponeschi7, E. Axiotis8, M. Carlesimo9, A. De Santis10, M. Fiorilli11, M. Casato12
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy. marcella.visentini@uniroma1.it
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Gastroenterology and Hepatology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- Division of Clinical Immunology, Department of Clinical Medicine, Sapienza University of Rome, Italy.
- 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.