Source:http://linkedlifedata.com/resource/pubmed/id/16973114
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2006-9-15
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pubmed:abstractText |
Recent progress in defining the role of genetic factors in rheumatoid arthritis (RA) has been remarkable. Anticyclic citrullinated peptide (anti-CCP) antibody-positive disease appears to be immunogenetically distinct from anti-CCP-negative disease, with the former subgroup primarily responsible for association and linkage with the HLA-DRB1 shared epitope (SE). There is preliminary evidence that non-HLA genes contribute differentially to anti-CCP-positive and negative disease. The phenotypic differences evident in anti-CCP-positive and negative disease suggest a need to reclassify RA based on the presence or absence of this autoantibody. Some recent work also suggests marked interactions between cigarette smoking, anti-CCP antibodies, and the SE, though these relationships may vary across populations. Lastly, a recent single nucleotide polymorphism-based genome-wide linkage analysis of multicase RA families revealed novel genomic regions that likely contain genes that predispose to RA or more specific phenotypes.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1523-3774
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
394-400
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pubmed:meshHeading | |
pubmed:year |
2006
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pubmed:articleTitle |
Recent advances in the genetics of rheumatoid arthritis.
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pubmed:affiliation |
Rosalind Russell Medical Research Center for Arthritis, University of California-San Francisco, 374 Parnassus Avenue, Box 0500, San Francisco, CA 94143-0500, USA.
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pubmed:publicationType |
Journal Article,
Review
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