Thus, it is postulated that the gene conferring predisposition to the development of AS is either HLA-B27 itself or another gene in very close proximity to the HLA-B locus.
However, AS patients with extraspinal disease were noted to have a significantly increased prevalence of the TAP 1B allele (17.0%) as compared to AS patients without extraspinal disease (2.9%) (P = 0.005) or normal controls (1.9%) (P = 0.005).
However, AS patients with extraspinal disease were noted to have a significantly increased prevalence of the TAP 1B allele (17.0%) as compared to AS patients without extraspinal disease (2.9%) (P = 0.005) or normal controls (1.9%) (P = 0.005).
However, AS patients with extraspinal disease were noted to have a significantly increased prevalence of the TAP 1B allele (17.0%) as compared to AS patients without extraspinal disease (2.9%) (P = 0.005) or normal controls (1.9%) (P = 0.005).
A polymorphic CfoI restriction enzyme site in the coding region of the LMP2 gene was evaluated in genomic DNA samples from 193 white and 49 Chinese B27 individuals with well documented AS, 97 of whom had had acute anterior uveitis (AAU) and 97 peripheral arthritis; 42 samples from normal, white, B27 positive blood donors in whom AS was excluded were also evaluated.
Serum antibodies from patients with ankylosing spondylitis and Reiter's syndrome are reactive with HLA-B27 cells transfected with the Mycobacterium tuberculosis hsp60 gene.
Serum antibodies from patients with ankylosing spondylitis and Reiter's syndrome are reactive with HLA-B27 cells transfected with the Mycobacterium tuberculosis hsp60 gene.
Because of the localization, in the proximity of the HLA-B locus, and the biological activities of TNF-alpha, we investigated the association between AS and a single base polymorphism located at position -308 of the TNF-alpha gene.
We studied TAP1 and TAP2 polymorphism in two multifactorial HLA-B27-associated diseases, ankylosing spondylitis (N = 30) and reactive arthritis (N = 30), in order to establish whether TAP genes are involved in the different pathogenesis of these diseases.
We studied TAP1 and TAP2 polymorphism in two multifactorial HLA-B27-associated diseases, ankylosing spondylitis (N = 30) and reactive arthritis (N = 30), in order to establish whether TAP genes are involved in the different pathogenesis of these diseases.