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Murine progressive ankylosis is not immunologically mediated
H E Krug1, M M Wietgrefe, S R Ytterberg
1Medicine Service, Veterans Affairs Medical Center (VAMC), Minneapolis, MN 55417, USA.
The Journal of Rheumatology
|January 1, 1997
Summary
This study found that the immune system does not cause murine progressive ankylosis, a condition similar to human spondyloarthropathies. Manipulations of the immune system did not affect the disease
Area of Science:
- Immunology
- Genetics
- Rheumatology
Background:
- Murine progressive ankylosis is an autosomal recessive disorder in mice.
- It shares similarities with human spondyloarthropathies.
- The gene responsible (ank) and its product are currently unknown.
Purpose of the Study:
- To investigate the role of the immune system in the pathogenesis of murine progressive ankylosis.
- To determine if immune cells or factors contribute to disease development.
Main Methods:
- Reciprocal transfers of spleen, bone marrow cells, or serum between affected (ank/ank) and normal mice.
- In vivo depletion of CD4 T cells using monoclonal antibodies.
- Breeding of ank/ank; nu/nu mice to assess the role of T and B lymphocytes.
Main Results:
- Immune system manipulations, including cell transfers and T cell depletion, did not alter the disease course.
- The development or severity of progressive ankylosis was not influenced by these immune interventions.
Conclusions:
- Progressive ankylosis in mice is not an immune-mediated disease.
- The observed similarities with human ankylosing spondylitis may stem from non-immune mechanisms driving osteogenesis in soft tissues.
