Background: The incidence and characteristics of spontaneous ankylosis in the ankle of specific F1 mice descended from two Fas-deficient strains were reported. Here the coincidence of synovial proliferation and ankylosis in the descendent F2 mice is reported.
Aim: To clarify whether the two distinct manifestations are genetically different.
Methods: An arthropathic group of mice (MCF2) were bred by intercrossing MRL/Mp.Faslpr-sap–/sap– and C3H/He.Faslpr mice. All mice were killed by bleeding under anaesthesia when they were 6 months old. Pathological grades for synovial proliferation were determined by microscopical examination. To obtain a linkage locus, the whole genome of male MCF2 mice was scanned by using 73 microsatellite markers.
Results: Synovial proliferation was equally observed in male and female MCF2 mice. No correlation was observed between the grades of synovial proliferation and the ankylosis occurring in the MCF2 mice. A suggestive susceptibility locus was shown in the middle of chromosome 11. This locus was an MRL allele with a recessive inheritance mode.
Conclusion: The pathogenic mechanisms of synovial proliferation and ankylosis are genetically different. The present locus is overlapped with some loci associated with rheumatoid arthritis and with others associated with experimental arthritides.
- MCF2, (MRL/rpl×C3H/lpr)F2
- SAP, signalling lymphocyte activation molecule-associated protein
- SLAM, signalling lymphocyte activation molecule
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↵* These authors contributed equally to this work.
Funding: This study was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan to SM (number 15390607) and MO (number 16390113).
Competing interests: None.
Published Online First 25 July 2006
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