PMID- 19730377
OWN - NLM
STAT- MEDLINE
DCOM- 20100304
LR  - 20111117
IS  - 1531-6963 (Electronic)
IS  - 1040-8711 (Linking)
VI  - 21
IP  - 6
DP  - 2009 Nov
TI  - An update on the immunogenetics of idiopathic inflammatory myopathies: major 
      histocompatibility complex and beyond.
PG  - 588-93
LID - 10.1097/BOR.0b013e3283315a22 [doi]
AB  - PURPOSE OF REVIEW: To update the reader on immunogenetic advances in idiopathic 
      inflammatory myopathy (IIM) over the past 18 months. RECENT FINDINGS: In 
      Caucasian IIM, despite a shared association with the human leukocyte antigen 
      (HLA) 8.1 ancestral haplotype (HLA-DRB1*03-DQA1*05-DQB1*02), anti-Jo-1 and 
      anti-PM-Scl antibody-positive cases have differing IIM clinical phenotypes. A 
      study of the HLA-DPB1 region has shown that DPB1*0101 is associated with 
      anti-Jo-1 positivity but not with anti-PM-Scl. IIM single nucleotide polymorphism 
      studies have demonstrated associations in the protein tyrosine phosphatase, 
      nonreceptor type 22, tumour necrosis factor alpha and interleukin-1 genes. The GM 
      13 allotype has been confirmed as a risk factor in Caucasian IIM. In inclusion 
      body myositis, the HLA 8.1 ancestral haplotype may not only influence disease 
      susceptibility but also disease expression. A follow-up study including a 
      meta-analysis of the apolipoprotein E gene in inclusion body myositis suggests 
      that this gene does not confer risk of disease. SUMMARY: Although a substantial 
      part of the genetic risk for developing adult and juvenile IIM lies within the 
      major histocompatibility complex, recent research suggests that genetic regions 
      outside of the major histocompatibility complex are also potentially involved in 
      conferring IIM disease susceptibility, although with more modest effect sizes. An 
      ongoing and internationally coordinated IIM genome-wide association scan may 
      provide further insights into IIM immunogenetics.
FAU - Chinoy, Hector
AU  - Chinoy H
AD  - The University of Manchester Rheumatic Diseases Centre, Salford Royal NHS 
      Foundation Trust, Salford, UK.
FAU - Lamb, Janine A
AU  - Lamb JA
FAU - Ollier, William E R
AU  - Ollier WE
FAU - Cooper, Robert G
AU  - Cooper RG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Curr Opin Rheumatol
JT  - Current opinion in rheumatology
JID - 9000851
RN  - 0 (Apolipoprotein E4)
RN  - 0 (Cytokines)
RN  - 0 (HLA-DP Antigens)
RN  - 0 (HLA-DP beta-Chains)
RN  - 0 (HLA-DPB1 antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (Immunoglobulin Gm Allotypes)
SB  - IM
MH  - Adult
MH  - Apolipoprotein E4/genetics
MH  - Child
MH  - Cytokines/genetics
MH  - Genetic Predisposition to Disease
MH  - HLA-DP Antigens/genetics
MH  - HLA-DP beta-Chains
MH  - HLA-DR Antigens/genetics
MH  - HLA-DRB1 Chains
MH  - Humans
MH  - Immunogenetic Phenomena
MH  - Immunoglobulin Gm Allotypes/genetics
MH  - *Major Histocompatibility Complex
MH  - Myositis/*genetics/*immunology
MH  - Myositis, Inclusion Body/genetics/immunology
MH  - Polymorphism, Single Nucleotide
RF  - 39
EDAT- 2009/09/05 06:00
MHDA- 2010/03/05 06:00
CRDT- 2009/09/05 06:00
PHST- 2009/09/05 06:00 [entrez]
PHST- 2009/09/05 06:00 [pubmed]
PHST- 2010/03/05 06:00 [medline]
AID - 10.1097/BOR.0b013e3283315a22 [doi]
PST - ppublish
SO  - Curr Opin Rheumatol. 2009 Nov;21(6):588-93. doi: 10.1097/BOR.0b013e3283315a22.