HLA–Bw60 increases susceptibility to ankylosing spondylitis in HLA–B27+ patients

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Abstract
We examined the distribution of non-B27 alleles of the HLA–B locus among B27+ patients with ankylosing spondylitis (AS), to detect any additional HLA–B locus allele(s) that may act in conjunction with B27 to increase susceptibility to AS. HLA–Bw60 (or B40 when the Bw60,61 split of B40 was not typed for) was shown to be increased among B27+ AS patients in each of 5 independent data sets. This increase was statistically significant in 4 of the 5 data sets studied, and the overall significance was P < 0.00001. Susceptibility to AS in B27+ individuals was further increased by a factor of ∼3 when Bw60 was also present. The distribution of HLA–A alleles on the B27-bearing haplotypes in AS patients was not significantly different from that in normal controls. On the other hand, the distribution of HLA–A alleles on Bw60-bearing haplotypes was significantly different from the distribution of A alleles on Bw60 haplotypes in the general population (P < 0.0005). Bw60 was not increased in B27- patients with AS. A dominant mode of inheritance generally fits AS; however, our sib pair analysis indicates that the B27, Bw60 disease subgroup follows a more recessive mode of inheritance.

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