Related Experiment Video
Updated: Jul 27, 2026
A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
Published on: November 9, 2017
HLA-B27 has no effect on the phenotypic expression of progressive ankylosis in ank/ank mice
1Department of Medicine, Department of Veterans Affairs Medical Center, and the University of Minnesota School of Medicine, Minneapolis, USA. krugx002@tc.umn.edu
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.
Insights
Human Leukocyte Antigen B27 (HLA-B27) does not influence murine progressive ankylosis (MPA) development in mice. The study suggests distinct disease processes for ankylosis and HLA-B27-associated conditions.
Area of Science:
- Immunogenetics
- Rheumatology
- Mouse Models of Disease
Background:
- Ankylosing spondylitis is a chronic inflammatory disease.
- Murine progressive ankylosis (MPA) is a genetic mouse model for ankylosis.
- The role of Human Leukocyte Antigen B27 (HLA-B27) in ankylosis is not fully understood.
Purpose of the Study:
- To determine if HLA-B27 influences the expression of murine progressive ankylosis (MPA).
- To investigate the interaction between HLA-B27 and the ank/ank genotype in a mouse model.
Main Methods:
- Breeding of HLA-B27 transgenic mice with ank/ank mice.
- Observation of F1 and F2 progeny phenotypes.
- Assessment of ankylosis development in relation to B27 status.
Main Results:
- Mice heterozygous for the ank gene (ank/+) showed no abnormalities.
- Mice homozygous for the ank gene (ank/ank) exhibited the typical MPA phenotype, regardless of B27 presence.
- HLA-B27 status did not alter the expression or severity of MPA.
Conclusions:
- Both HLA-B27 and the ank/ank genotype are independent risk factors for bony ankylosis.
- The disease processes associated with HLA-B27 and MPA appear distinct and noninteractive.
- These findings do not support a role for the human homolog of the ank locus in ankylosing spondylitis pathogenesis.
