HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice.
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.


CONCLUSIONS
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.
Krug
H E
HE
Department of Medicine, Department of Veterans Affairs Medical Center, and the University of Minnesota School of Medicine, Minneapolis, USA. krugx002@tc.umn.edu
Taurog
J D
JD
D000818:Animals; D000844:Ankylosis / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D015796:HLA-B27 Antigen / Q000235:genetics*; D006801:Humans; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010641:Phenotype
D015796:HLA-B27 Antigen