Studies of HLA-B27-associated disease.
Several rheumatic diseases were first shown to be associated with human leukocytic antigen (HLA)-B27 in 1973. Recent developments in understanding this association include the finding that there are at least six variants of HLA-B27 at the molecular level, with no one variant preferentially associated with disease. Detailed studies of the structure of the HLA-B27 molecular family are in progress in several laboratories. Mice expressing HLA-B27 and transmitting it to their offspring (transgenic mice) have been produced and are being studied for their response to bacteria that are known to trigger reactive arthritis in B27+ humans. A particular restriction fragment length polymorphism was recently claimed to be a genetic marker for an additional risk factor in ankylosing spondylitis, but two other laboratories have failed to confirm this finding.
Taurog
J D
JD
Harold C. Simmons Arthritis Research Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.
Durand
J P
JP
el-Zaatari
F A
FA
Hammer
R E
RE
D000818:Animals; D015252:Deoxyribonucleases, Type II Site-Specific; D008040:Genetic Linkage; D015235:HLA-B Antigens / Q000235:genetics*; D015796:HLA-B27 Antigen; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic / Q000235:genetics; D012150:Polymorphism, Restriction Fragment Length; D013167:Spondylitis, Ankylosing / Q000235:genetics*
D015235:HLA-B Antigens; D015796:HLA-B27 Antigen; C025630:CAGCTG-specific type II deoxyribonucleases; D015252:Deoxyribonucleases, Type II Site-Specific