PMID- 11092196
OWN - NLM
STAT- MEDLINE
DCOM- 20010524
LR  - 20190915
IS  - 1040-8711 (Print)
IS  - 1040-8711 (Linking)
VI  - 12
IP  - 6
DP  - 2000 Nov
TI  - Update on the genetics of the idiopathic inflammatory myopathies.
PG  - 482-91
AB  - 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.
FAU - Shamim, E A
AU  - Shamim EA
AD  - Division of Monoclonal Antibodies, Center for Biologics Evaluation and Research, 
      Food and Drug Administration, Bethesda, Maryland 20892, USA. shamim@cber.fda.gov
FAU - Rider, L G
AU  - Rider LG
FAU - Miller, F W
AU  - Miller FW
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (HLA Antigens)
SB  - IM
MH  - Autoimmune Diseases/genetics
MH  - HLA Antigens/genetics
MH  - Humans
MH  - Myositis/epidemiology/*genetics
MH  - Risk Factors
RF  - 87
EDAT- 2000/11/25 11:00
MHDA- 2001/05/26 10:01
CRDT- 2000/11/25 11:00
PHST- 2000/11/25 11:00 [pubmed]
PHST- 2001/05/26 10:01 [medline]
PHST- 2000/11/25 11:00 [entrez]
AID - 10.1097/00002281-200011000-00002 [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2000 Nov;12(6):482-91. doi: 
      10.1097/00002281-200011000-00002.