PMID- 11094432
OWN - NLM
STAT- MEDLINE
DCOM- 20010315
LR  - 20220408
IS  - 1465-9905 (Print)
IS  - 1465-9913 (Electronic)
IS  - 1465-9905 (Linking)
VI  - 2
IP  - 3
DP  - 2000
TI  - Association of MHC and rheumatoid arthritis. HLA polymorphisms in phenotypic 
      variants of rheumatoid arthritis.
PG  - 212-6
AB  - Genes in the human leukocyte antigen (HLA) region remain the most powerful 
      disease risk genes in rheumatoid arthritis (RA). Several allelic variants of 
      HLA-DRB1 genes have been associated with RA, supporting a role for T-cell 
      receptor-HLA-antigen interactions in the pathologic process. Disease-associated 
      HLA-DRB1 alleles are similar but not identical and certain allelic variants are 
      preferentially enriched in patient populations with defined clinical 
      characteristics. Also, a gene dosing effect of HLA-DRB1 alleles has been 
      suggested by the accumulation of patients with two RA-associated alleles, 
      especially in patient subsets with a severe disease course. Therefore, 
      polymorphisms in HLA genes are being explored as tools to dissect the clinical 
      heterogeneity of the rheumatoid syndrome. Besides HLA polymorphisms, other risk 
      genes will be helpful in defining genotypic profiles correlating with disease 
      phenotypes. One such phenotype is the type of synovial lesion generated by the 
      patient. HLA genes in conjunction with other genetic determinants may predispose 
      patients to a certain pathway of synovial inflammation. Also, patients may or may 
      not develop extraarticular manifestations, which are critical in determining 
      morbidity and mortality. HLA genes, complemented by other RA risk genes, are 
      likely involved in shaping the T-cell repertoire, including the emergence of an 
      unusual T-cell population characterized by the potential of vascular injury, such 
      as seen in extraarticular RA.
FAU - Weyand, C M
AU  - Weyand CM
AD  - Department of Medicine, Mayo Clinic Foundation, Rochester, Minnesota 55905, USA. 
      weyand.cornelia@mayo.edu
FAU - Goronzy, J J
AU  - Goronzy JJ
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20000419
PL  - England
TA  - Arthritis Res
JT  - Arthritis research
JID - 100913255
RN  - 0 (HLA Antigens)
SB  - IM
CIN - Arthritis Res. 2000;2(3):203-4. PMID: 11094429
MH  - Arthritis, Rheumatoid/*genetics/*immunology
MH  - HLA Antigens/*genetics/immunology
MH  - Humans
MH  - Major Histocompatibility Complex/*genetics/immunology
MH  - Phenotype
MH  - Polymorphism, Genetic/*immunology
PMC - PMC130005
EDAT- 2000/11/30 11:00
MHDA- 2001/03/17 10:01
PMCR- 2000/04/19
CRDT- 2000/11/30 11:00
PHST- 2000/01/19 00:00 [received]
PHST- 2000/02/29 00:00 [accepted]
PHST- 2000/11/30 11:00 [pubmed]
PHST- 2001/03/17 10:01 [medline]
PHST- 2000/11/30 11:00 [entrez]
PHST- 2000/04/19 00:00 [pmc-release]
AID - ar90 [pii]
AID - 10.1186/ar90 [doi]
PST - ppublish
SO  - Arthritis Res. 2000;2(3):212-6. doi: 10.1186/ar90. Epub 2000 Apr 19.