[Genomic approaches to bone and joint diseases. Current status of human disease genomics in rheumatoid arthritis].
Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder which causes progression of polyarticular destruction. RA is a multifactorial disorder, in which genetic and environmental factors contribute to the onset of diseases. Linkage analyses and case-control association studies in RA have identified several susceptible genes including genetic variation in human leukocyte antigen region. Here, we review major genes susceptible to RA, and discuss effects of these genes on production of anti-cyclic citrullinated peptides antibody.
Shimane
Kenichi
K
Institute of Physical and Chemical Research (RIKEN), SNP Research Center, Laboratory for Rheumatic Diseases/the University of Tokyo, Graduate School of Medicine, Department of Allergy and Rheumatology.
Yamamoto
Kazuhiko
K
Kochi
Yuta
Y
D001172:Arthritis, Rheumatoid / Q000235:genetics*; D006680:HLA Antigens / Q000235:genetics*; D006801:Humans; D006867:Hydrolases / Q000235:genetics; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22 / Q000235:genetics; D000080002:Protein-Arginine Deiminase Type 4; D000076342:Protein-Arginine Deiminases; D011971:Receptors, Immunologic / Q000235:genetics; D047990:TNF Receptor-Associated Factor 1 / Q000235:genetics
C457775:FCRL3 protein, human; D006680:HLA Antigens; D011971:Receptors, Immunologic; D047990:TNF Receptor-Associated Factor 1; D006867:Hydrolases; C516765:PTPN22 protein, human; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22; C000629235:PADI4 protein, human; D000080002:Protein-Arginine Deiminase Type 4; D000076342:Protein-Arginine Deiminases