Linked Life Data

10761560

Source:http://linkedlifedata.com/resource/pubmed/id/10761560

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-5-2
pubmed:abstractText
Studies of mixed cryoglobulins (MC) from patients infected with hepatitis C virus (HCV) show that the principal constituents in cryoprecipitate are IgM rheumatoid factors (RF), polyclonal IgG anti-HCV antibodies, and HCV RNA. The HCV-induced RF response is biased to produce IgM RF encoded by a restricted set of Ig V genes, predominantly the VH/VL gene pair 51p1/kv325. The propensity of such IgM RF to cryoprecipitate is likely a coincidental property of their V region sequences, but the clinical effect of this bias is increased by the persistence of circulating HCV-IgG immune complexes. These complexes might induce production of cryoprecipitable IgM RF and furnish multi-molecular structures that favor binding by cryoprecipitable IgM RF. The V gene sequences of HCV-induced IgM RF have features seen in other RF responses, suggesting a common immunological mechanism that is independent of HCV. B cell proliferation is probably enhanced by HCV-specific properties, however, including the ability of HCV proteins to bind to CD81 on the B cell surface, and to influence intracellular regulatory functions following viral entry into B cells. The V gene bias in HCV-induced RF is most apparent among the B cells in monoclonal expansions responsible for type II cryoglobulins, but it might originate early the polyclonal RF response, before MC are detectable. Monoclonal B cell expansions and lymphomatoid bone marrow infiltrates in HCV+ patients predominantly involve CD5-negative IgM RF B cells. Non-RF B cells can also be expanded, including producers of IgG1 and IgG3 that are likely anti-HCV antibodies. The initial site of B cell clonal expansion may be in the liver, where lymphoid aggregates are abundant and RF are produced. Sorting out how MC formation is influenced by properties that are inherent to the RF response, or specific to HCV infection, will be a challenge to future HCV research.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigen-Antibody Complex, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD81, http://linkedlifedata.com/resource/pubmed/chemical/CD81 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Cryoglobulins, http://linkedlifedata.com/resource/pubmed/chemical/Hepatitis C Antibodies, http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G, http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Viral, http://linkedlifedata.com/resource/pubmed/chemical/Rheumatoid Factor, http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0003-410X
pubmed:author
pubmed:issnType
Print
pubmed:volume
151
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
30-40
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
The rheumatoid factor response in the etiology of mixed cryoglobulins associated with hepatitis C virus infection.
pubmed:affiliation
Department of Medicine, University of Washington, Seattle 98105, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't