Clonal expansion of immunoglobulin M+CD27+ B cells in HCV-associated mixed cryoglobulinemia

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 pro-liferation of B cells. Here we demonstrat...

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Bibliographic Details
Published inBlood Vol. 111; no. 3; pp. 1344 - 1356
Main Authors Charles, Edgar D., Green, Rashidah M., Marukian, Svetlana, Talal, Andrew H., Lake-Bakaar, Gerond V., Jacobson, Ira M., Rice, Charles M., Dustin, Lynn B.
Format Journal Article
LanguageEnglish
Published Washington, DC Elsevier Inc 01.02.2008
The Americain Society of Hematology
American Society of Hematology
SeriesImmunobiology
Subjects
Adult
B-Lymphocytes - immunology
Biological and medical sciences
Cryoglobulinemia - etiology
Cryoglobulinemia - genetics
Cryoglobulinemia - immunology
Female
Hepacivirus - immunology
Human viral diseases
Humans
Immunobiology
Immunodeficiencies. Immunoglobulinopathies
Immunoglobulin M - classification
Immunoglobulin M - genetics
Immunoglobulin M - immunology
Immunoglobulinopathies
Immunopathology
Infectious diseases
Male
Medical sciences
Middle Aged
Phenotype
Phylogeny
Receptors, Complement 3d - immunology
Tumor Necrosis Factor Receptor Superfamily, Member 7 - immunology
Viral diseases
Viral hepatitis
Human
Immunopathology
Immune response
Pathogenesis
Mixed cryoglobulinemia
Hepatic disease
B-Lymphocyte
Clonal expansion
IgM
Infection
Virus
Somatic mutation
Immunoglobulinopathy
Viral disease
Digestive diseases
Flaviviridae
Hepatitis C virus
Hepacivirus
Humoral immunity
Monoclonal immunoglobulin
Viral hepatitis C
Online AccessGet full text
ISSN0006-4971
1528-0020
DOI10.1182/blood-2007-07-101717

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Abstract 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 pro-liferation of B cells. Here we demonstrate that certain HCV+MC+ subjects have clonal expansions of immunoglobulin M (IgM)+κ+IgDlow/−CD21lowCD27+ 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 Vκ3-20 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.
AbstractList 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 pro-liferation of B cells. Here we demonstrate that certain HCV+MC+ subjects have clonal expansions of immunoglobulin M (IgM)+κ+IgDlow/−CD21lowCD27+ 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 Vκ3-20 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.
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 pro-liferation of B cells. Here we demonstrate that certain HCV + MC + subjects have clonal expansions of immunoglobulin M (IgM) + κ + IgD low/− CD21 low CD27 + B cells. Using RT-PCR to amplify Ig from these singly sorted cells, we show that these predominantly rheumatoid factor-encoding V H 1-69/J H 4 and V κ 3-20 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.
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 pro-liferation of B cells. Here we demonstrate that certain HCV(+)MC(+) subjects have clonal expansions of immunoglobulin M (IgM)(+)kappa(+)IgD(low/-)CD21(low)CD27(+) B cells. Using RT-PCR to amplify Ig from these singly sorted cells, we show that these predominantly rheumatoid factor-encoding V(H)1-69/J(H)4 and V(kappa)3-20 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.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 pro-liferation of B cells. Here we demonstrate that certain HCV(+)MC(+) subjects have clonal expansions of immunoglobulin M (IgM)(+)kappa(+)IgD(low/-)CD21(low)CD27(+) B cells. Using RT-PCR to amplify Ig from these singly sorted cells, we show that these predominantly rheumatoid factor-encoding V(H)1-69/J(H)4 and V(kappa)3-20 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.
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 pro-liferation of B cells. Here we demonstrate that certain HCV(+)MC(+) subjects have clonal expansions of immunoglobulin M (IgM)(+)kappa(+)IgD(low/-)CD21(low)CD27(+) B cells. Using RT-PCR to amplify Ig from these singly sorted cells, we show that these predominantly rheumatoid factor-encoding V(H)1-69/J(H)4 and V(kappa)3-20 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.
Author Rice, Charles M.
Green, Rashidah M.
Charles, Edgar D.
Lake-Bakaar, Gerond V.
Marukian, Svetlana
Dustin, Lynn B.
Talal, Andrew H.
Jacobson, Ira M.
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– sequence: 2
  givenname: Rashidah M.
  surname: Green
  fullname: Green, Rashidah M.
  organization: Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, Rockefeller University, New York, NY; and
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  givenname: Svetlana
  surname: Marukian
  fullname: Marukian, Svetlana
  organization: Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, Rockefeller University, New York, NY; and
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  givenname: Andrew H.
  surname: Talal
  fullname: Talal, Andrew H.
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  surname: Jacobson
  fullname: Jacobson, Ira M.
  organization: Department of Medicine, Division of Gastroenterology and Hepatology, Weill Medical College of Cornell University, New York, NY
– sequence: 7
  givenname: Charles M.
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  fullname: Rice, Charles M.
  organization: Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, Rockefeller University, New York, NY; and
– sequence: 8
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  surname: Dustin
  fullname: Dustin, Lynn B.
  email: dustinl@rockefeller.edu
  organization: Center for the Study of Hepatitis C, Laboratory of Virology and Infectious Disease, Rockefeller University, New York, NY; and
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IsScholarly true
Issue 3
Keywords Human
Immunopathology
Immune response
Pathogenesis
Mixed cryoglobulinemia
Hepatic disease
B-Lymphocyte
Clonal expansion
IgM
Infection
Virus
Somatic mutation
Immunoglobulinopathy
Viral disease
Digestive diseases
Flaviviridae
Hepatitis C virus
Hepacivirus
Humoral immunity
Monoclonal immunoglobulin
Viral hepatitis C
Language English
License This article is made available under the Elsevier license.
CC BY 4.0
LinkModel OpenURL
MergedId FETCHMERGED-LOGICAL-c487t-96e46389dbd844162959b0c904cb6de0fc25ce106fe6b39cf4ae14befd8741053
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
OpenAccessLink https://dx.doi.org/10.1182/blood-2007-07-101717
PMID 17942751
PQID 70242890
PQPubID 23479
PageCount 13
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_2214737
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crossref_citationtrail_10_1182_blood_2007_07_101717
crossref_primary_10_1182_blood_2007_07_101717
elsevier_sciencedirect_doi_10_1182_blood_2007_07_101717
ProviderPackageCode CITATION
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PublicationCentury 2000
PublicationDate 2008-02-01
PublicationDateYYYYMMDD 2008-02-01
PublicationDate_xml – month: 02
  year: 2008
  text: 2008-02-01
  day: 01
PublicationDecade 2000
PublicationPlace Washington, DC
PublicationPlace_xml – name: Washington, DC
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PublicationSeriesTitle Immunobiology
PublicationTitle Blood
PublicationTitleAlternate Blood
PublicationYear 2008
Publisher Elsevier Inc
The Americain Society of Hematology
American Society of Hematology
Publisher_xml – name: Elsevier Inc
– name: The Americain Society of Hematology
– name: American Society of Hematology
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Snippet Hepatitis C virus (HCV) is associated with B-cell lymphoproliferative disorders such as mixed cryoglobulinemia (MC) and B-cell non-Hodgkin lymphoma (B-NHL)....
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SubjectTerms Adult
B-Lymphocytes - immunology
Biological and medical sciences
Cryoglobulinemia - etiology
Cryoglobulinemia - genetics
Cryoglobulinemia - immunology
Female
Hepacivirus - immunology
Human viral diseases
Humans
Immunobiology
Immunodeficiencies. Immunoglobulinopathies
Immunoglobulin M - classification
Immunoglobulin M - genetics
Immunoglobulin M - immunology
Immunoglobulinopathies
Immunopathology
Infectious diseases
Male
Medical sciences
Middle Aged
Phenotype
Phylogeny
Receptors, Complement 3d - immunology
Tumor Necrosis Factor Receptor Superfamily, Member 7 - immunology
Viral diseases
Viral hepatitis
Title Clonal expansion of immunoglobulin M+CD27+ B cells in HCV-associated mixed cryoglobulinemia
URI https://dx.doi.org/10.1182/blood-2007-07-101717
https://www.ncbi.nlm.nih.gov/pubmed/17942751
https://www.proquest.com/docview/70242890
https://pubmed.ncbi.nlm.nih.gov/PMC2214737
Volume 111
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