Objective, Murine progressive ankylosis is an autosomal recessive diso
rder in mice similar to the human spondyloarthropathies. The gene resp
onsible for progressive ankylosis, ank, has not been identified and it
s product is unknown. We investigated whether the immune system plays
a role in the pathogenesis of progressive ankylosis. Methods, Reciproc
al transfers of spleen or bone marrow cells or serum between ank/ank a
nd normal mice were performed. CD4 T cells were depleted in vivo by in
jection with monoclonal antibody. Ank/ank; nu/nu mice were bred from d
ouble heterozygote offspring of homozygote parents. Results, Disease w
as neither ameliorated nor induced by these immune system manipulation
s. Conclusion, We conclude that progressive ankylosis is not immune me
diated. The similarities between ankylosing spondylitis and murine pro
gressive ankylosis may be due to mechanisms producing osteogenesis in
nonosseous tissues.