TAP2 ALLELES IN INFLAMMATORY ARTHRITIS

Sixty patients with reactive arthritis (ReA) and 40 with rheumatoid ar thritis (RA), were typed for HLA-B27 and class II antigens DR and DQ, and studied for TAP2 gene polymorphism in comparison with 60 healthy c ontrols. TAP2 polymorphisms at positions 379, 565, 665, and 687 were a nalyzed using amplification refractory system-based PCR and polymorphi sms at positions 386 and 651 using oligonucleotide hybridization. The frequency of the TAP2A/A genotype was 30% (12/40) in RA, in contrast t o 13% (8/60) in the controls. This genotype was further associated wit h DRBI04 positive RA (10/24, 42%, P= 0.01), as well as the TAP2A alle le (31/48, 65%, P = 0.012). Thr/Thr dimorphism at TAP2 position 665 (2 4/40, 60%, P=0.024) and Stop/Stop dimorphism at TAP2 position 687 (24/ 40, 60%, P=0.024) were found to be increased in RA patients as compare d to controls. When TAP2I/J polymorphism was studied, TAP2J positivity was found associated with the HLA-B27 DR4-DQB10301-haplotype in ReA patients. 9/12 of these were positive as compared to 20/60 in random c ontrols (P = 0.010). Polymorphisms of the TAP2 gene were found to be a ssociated with subgroups of RA and ReA patients with disease associate d markers (e.g. TAP2A in DRB104 positive RA, or TAP2J in HLA-B27-DRB1 04-DQB1*0301 positive ReA). These may thus serve as additional marker s of specific haplotypes associated with susceptibility to inflammator y arthritis.