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Blood, 1 February 2008, Vol. 111, No. 3, pp. 1344-1356. Prepublished online as a Blood First Edition Paper on October 17, 2007; DOI 10.1182/blood-2007-07-101717. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2007-07-101717v1 111/3/1344    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Charles, E. D. Articles by Dustin, L. B. Search for Related Content PubMed PubMed Citation Articles by Charles, E. D. Articles by Dustin, L. B. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 17, 2007 Accepted October 12, 2007 Clonal expansion of IgM+CD27+ B cells in HCV-associated mixed cryoglobulinemia Edgar D. Charles, Rashidah M. Green, Svetlana Marukian, Andrew H. Talal, Gerond V. Lake-Bakaar, Ira M. Jacobson, Charles M Rice, and Lynn B. Dustin* Center for the Study of Hepatitis C, The Rockefeller University, New York, NY, United States Dept. of Medicine, Div. of Gastroenterology and Hepatology, Weill Medical College of Cornell University, New York, NY, United States * Corresponding author; email: dustinl{at}rockefeller.edu. Hepatitis C virus (HCV) is associated with B cell lymphoproliferative disorders such as mixed cryoglobulinemia (MC) and B cell non-Hodgkin lymphoma (B-NHL). The pathogenesis of these disorders remains unclear, and it has been proposed that HCV drives the proliferation of B cells. Here we demonstrate that certain HCV+MC+ subjects have clonal expansions of IgM++IgDlow/negCD21lowCD27+ B cells. Using RT-PCR to amplify Ig from these singly-sorted cells, we show that these predominantly rheumatoid factor-encoding VH1-69/JH4 and V3-20 gene segment-restricted cells have low to moderate levels of somatic hypermutations. Ig sequence analysis suggests that antigen selection drives the generation of mutated clones. These findings lend further support to the notion that specific antigenic stimulation leads to B cell proliferation in HCV MC and that chronic B cell stimulation may set the stage for malignant transformation and the development of B-NHL. The finding that these hypermutated, marginal zone-like IgM+CD27+ B cells are clonally expanded in certain subjects with MC offers insight into mechanisms of HCV-associated MC and B cell malignancy. This study was registered at www.clinicaltrials.gov as #NCT00219999. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Paulli, L. Arcaini, M. Lucioni, E. Boveri, D. Capello, F. Passamonti, M. Merli, S. Rattotti, D. Rossi, R. Riboni, et al. Subcutaneous 'lipoma-like' B-cell lymphoma associated with HCV infection: a new presentation of primary extranodal marginal zone B-cell lymphoma of MALT Ann. Onc., October 25, 2009; (2009) mdp454v1. [Abstract] [Full Text] [PDF] D. B. Cines, J. B. Bussel, H. A. Liebman, and E. T. Luning Prak The ITP syndrome: pathogenic and clinical diversity Blood, June 25, 2009; 113(26): 6511 - 6521. [Abstract] [Full Text] [PDF] E. Bigot-Corbel, M. Gassin, I. Corre, D. Le Carrer, O. Delaroche, and S. Hermouet Hepatitis C virus (HCV) infection, monoclonal immunoglobulin specific for HCV core protein, and plasma-cell malignancy Blood, November 15, 2008; 112(10): 4357 - 4358. [Full Text] [PDF]

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