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A non-major histocompatibility locus determines tissue specificity in the pathogenic process underlying synovial proliferation in a mouse arthropathy model


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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