Objective. To investigate whether HLA-B27 influences the expression of murine progressive ankylosis (MPA), a single-gene autosomal recessive mouse model of ankylosing spondylitis that arises in mice homozygous for the ank gene. Methods. Mice transgenic for HLA-B27 were bred with ank/ank mice, and the phenotypes of the F1 and F2 progeny were observed. Results. ank/+ mice showed no abnormalities, and ank/ank mice showed the typical phenotype of MPA, irrespective of B27 status. Conclusion. HLA-B27 and the ank/ank genotype both predispose to diseases involving progressive bony ankylosis. These findings suggest that these disease processes are distinct and noninteractive, and they provide no support for the hypothesis that the human homolog of the ank locus participates in the pathogenesis of ankylosing spondylitis.
|Original language||English (US)|
|Number of pages||3|
|Journal||Journal of Rheumatology|
|State||Published - 2000|
- Mice transgenic