Abstract
Symmetrical lupoid onychodystrophy (SLO) is an immune-mediated disease in dogs affecting the claws with a suggested autoimmune aethiology. Sequence-based genotyping of the polymorphic exon 2 from DLA-DRB1, -DQA1, and -DQB1 class II loci were performed in a total of 98 SLO Gordon setter cases and 98 healthy controls. A risk haplotype (DRB1*01801/DQA1*00101/DQB1*00802) was present in 53% of cases and 34% of controls and conferred an elevated risk of developing SLO with an odds ratio (OR) of 2.1. When dogs homozygous for the risk haplotype were compared to all dogs not carrying the haplotype the OR was 5.4. However, a stronger protective haplotype (DRB1*02001/DQA1*00401/DQB1*01303, OR = 0.03, 1/OR = 33) was present in 16.8% of controls, but only in a single case (0.5%). The effect of the protective haplotype was clearly stronger than the risk haplotype, since 11.2% of the controls were heterozygous for the risk and protective haplotypes, whereas this combination was absent from cases. When the dogs with the protective haplotype were excluded, an OR of 2.5 was obtained when dogs homozygous for the risk haplotype were compared to those heterozygous for the risk haplotype, suggesting a co-dominant effect of the risk haplotype. In smaller sample sizes of the bearded collie and giant schnauzer breeds we found the same or similar haplotypes, sharing the same DQA1 allele, over-represented among the cases suggesting that the risk is associated primarily with DLA-DQ. We obtained conclusive results that DLA class II is significantly associated with risk of developing SLO in Gordon setters, thus supporting that SLO is an immune-mediated disease. Further studies of SLO in dogs may provide important insight into immune privilege of the nail apparatus and also knowledge about a number of inflammatory disorders of the nail apparatus like lichen planus, psoriasis, alopecia areata and onycholysis.
Highlights
Canine symmetrical lupoid onychodystrophy (SLO) is described as separation and sloughing of several claws from claw beds and affecting all claws
In the present study we have evaluated the association of major histocompatibility complex (MHC) class II haplotypes and alleles with symmetrical lupoid onychodystrophy in a large cohort of Gordon setter and smaller numbers from two additional breeds of dogs, the giant schnauzer and the bearded collie
The analysis revealed that DLA class II is significantly associated with SLO and provides support for the hypothesis of SLO being an immune-mediated disease
Summary
Canine symmetrical lupoid onychodystrophy (SLO) is described as separation and sloughing of several claws from claw beds and affecting all claws. The pathogenesis of SLO is incompletely elucidated, but allergic, infectious and immunemediated diseases have all been associated with symmetrical onychomadesis [1]. The lupoid reaction observed histopathologically and the clinical signs of onychomadesis represent an immune-mediated disease of the claw, rather than an actual triggering event of the disease. Separation of claw from claw bed and subsequent sloughing is noted on one or more claws, but within two to three months all claws might be affected. Histopathology of affected claws present infiltrates of mononuclear cells, apoptosis of the epidermal basal cells and hydropic degeneration of the epidermal basal cells. Treatment with immunosuppressive drugs, such as glucocorticoids, has been reported to be successful [5] as well as fatty acid supplementation [6] suggesting an autoimmune aethiology of the disease
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