Linked Life Data

11092196

Source:http://linkedlifedata.com/resource/pubmed/id/11092196

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2000-11-28
pubmed:abstractText
A number of lines of investigation suggest that, as is likely the case for other autoimmune diseases, the idiopathic inflammatory myopathies (IIM) develop as a result of specific environmental exposures in genetically susceptible individuals. Current data imply that multiple genes are involved in the etiology of these complex disorders. Targeted gene studies and whole genome approaches have begun to identify several genetic risk factors for autoimmune diseases, but the rarity and heterogeneity of the IIM have limited our knowledge of their associated genes. Current findings suggest that human leukocyte antigen (HLA) genes on chromosome 6, particularly HLA DRB1*0301 and the linked allele DQA1*0501, have the strongest associations with all clinical forms of IIM in white patients. Different HLA alleles, however, may confer risk or protection for myositis in distinct ethnic, serologic, and environmental exposure groups. Non-HLA genetic risk factors, which have been documented for other autoimmune diseases, are now being identified for the IIM. These include polymorphic genes encoding immunoglobulin heavy chains (defined by serologic markers known as Gm allotypes), cytokines and their receptors, and certain proteins that accumulate in the myocyte vacuoles of inclusion body myositis patients. Selected allelic polymorphisms of interleukin-1 receptor antagonist variable number tandem repeats and genes for tumor necrosis factor alpha and interleukin-1 alpha also have recently been associated with IIM. The pathogenic bases for the differences among the many clinically, pathologically and immunologically defined syndromes known as the IIM will be elucidated through a better understanding of the multiple genes that define risks for their development, as well as through investigations of gene-gene and gene-environment interactions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1040-8711
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
482-91
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Update on the genetics of the idiopathic inflammatory myopathies.
pubmed:affiliation
Division of Monoclonal Antibodies, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA. shamim@cber.fda.gov
pubmed:publicationType
Journal Article, Review