Expansion of peripheral blood CD81/CD5+ B cells and its relation to disease severity and autoimmune markers in chronic HCV infection

2001 ◽  
Vol 34 (0) ◽  
pp. 126
Author(s):  
E Zuckerman
2001 ◽  
Vol 34 ◽  
pp. 126
Author(s):  
E. Zuckerman ◽  
G. Slobodin ◽  
A. Kessel ◽  
E. Sabo ◽  
D. Yeshurun ◽  
...  

2018 ◽  
Vol 193 (2) ◽  
pp. 183-193 ◽  
Author(s):  
N. Eiza ◽  
E. Zuckerman ◽  
M. Carlebach ◽  
T. Rainis ◽  
Y. Goldberg ◽  
...  

2001 ◽  
Vol 31 (8) ◽  
pp. 2388-2394 ◽  
Author(s):  
Anna M. Grabowska ◽  
Franziska Lechner ◽  
Paul Klenerman ◽  
Paddy J. Tighe ◽  
Stephen Ryder ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Masahiko Ito ◽  
Hideki Kusunoki ◽  
Keiko Mochida ◽  
Kazunari Yamaguchi ◽  
Toshiaki Mizuochi

Hepatitis C virus (HCV) has been recognized as a major cause of chronic liver diseases worldwide. It has been suggested that HCV infects not only hepatocytes but also mononuclear lymphocytes including B cells that express the CD81 molecule, a putative HCV receptor. HCV infection of B cells is the likely cause of B-cell dysregulation disorders such as mixed cryoglobulinemia, rheumatoid factor production, and B-cell lymphoproliferative disorders that may evolve into non-Hodgkin's lymphoma (NHL). Epidemiological data indicate an association between HCV chronic infection and the occurrence of B-cell NHL, suggesting that chronic HCV infection is associated at least in part with B-cell lymphomagenesis. In this paper, we aim to provide an overview of recent literature, including our own, to elucidate a possible role of HCV chronic infection in B-cell lymphomagenesis.


2010 ◽  
Vol 52 ◽  
pp. S275
Author(s):  
E. Zuckerman ◽  
C. Dashkovsky ◽  
R. Peri ◽  
E. Sabo ◽  
E. Toubi

2001 ◽  
Vol 75 (3) ◽  
pp. 1229-1235 ◽  
Author(s):  
David K. H. Wong ◽  
Darryll D. Dudley ◽  
Paul B. Dohrenwend ◽  
Georg M. Lauer ◽  
Raymond T. Chung ◽  
...  

ABSTRACT Broadly directed hepatitis C virus (HCV)-specific cytotoxic T lymphocytes (CTL) have been identified from liver-infiltrating lymphocytes but have been more difficult to assess in peripheral blood of infected persons. To enhance the detection of CTL from peripheral blood mononuclear cells (PBMC), we cocultured PBMC with autologous Epstein-Barr virus-transformed B-lymphoblastoid cell lines that had been infected with recombinant vaccinia virus constructs so that they expressed the entire translated polyprotein of HCV-H, a type 1a strain. These stimulated cells from HCV-infected as well as exposed seronegative persons were then cloned at limiting dilution and tested for HCV-specific CTL activity using a standard 51Cr release assay. HCV-specific CTL were detected in PBMC from seven of nine persons with chronic hepatitis, including five of seven in whom CTL had previously been detected from liver biopsy specimens but not PBMC. In a single person with chronic HCV infection, CTL directed against as many as five different epitopes were detected in peripheral blood and were similar in specificity to those detected in liver tissue. This technique was used to evaluate eight subjects identified to be at high risk for HCV exposure due to continued injection drug abuse; no evidence of CTL in PBMC was found. We conclude that CTL can be detected in PBMC from the majority of persons with chronic HCV infection but are present at lower levels or absent in exposed but persistently seronegative persons. The high degree of concordance of HCV epitopes identified from liver and PBMC suggests that this strategy is a reasonable alternative to liver biopsy for characterizing the CTL response to HCV in chronically infected persons.


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