Objective. Murine progressive ankylosis is an autosomal recessive disorder in mice similar to the human spondyloarthropathies. The gene responsible for progressive ankylosis, ank, has not been identified and its product is unknown. We investigated whether the immune system plays a role in the pathogenesis of progressive ankylosis. Methods. Reciprocal transfers of spleen or bone marrow cells or serum between ank/ank and normal mice were performed. CD4 T cells were depleted in vivo by injection with monoclonal antibody. Ank/ank; nu/nu mice were bred from double heterozygote offspring of homozygote parents. Results. Disease was neither ameliorated nor induced by these immune system manipulations. Conclusion. We conclude that progressive ankylosis is not immune mediated. The similarities between ankylosing spondylitis and murine progressive ankylosis may be due to mechanisms producing osteogenesis in nonosseous tissues.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Rheumatology|
|State||Published - Jan 1 1997|
- animal disease models