Atopic dermatitis (AD) is a chronic inflammatory and pruritic skin disease commonly seen in dogs and humans. Most cases involve hypersensitivity to the house
dust mites Dertnatophagoides farinae and D. pteronyssinus. This study has shown
that Dermatophagoides specific IgE and peripheral blood mononuclear cell (PBMC)
responses were largely restricted to skin test positive atopic dogs. Furthermore, immunoblotting and PBMC proliferation studies demonstrated that the major target of
immune recognition is a 98/104kD protein, rather than the low molecular weight
group 1 and 2 proteins important in humans. The close association between serological findings and PBMC proliferation implies that T-cells participate in the pathogenesis of canine AD by supporting IgE production. Human AD is associated with
T-helper 2 (TH2) type responses, although THi cytokines are present in chronic lesions. In contrast, tolerance in healthy individuals is mediated by regulatory T-cells.
Using semi-quantitative reverse transcriptase-polymerase chain reactions, this study
found that canine AD is associated with over-production of the TH2 cytokine interleukin (IL)-4, whilst tolerance in healthy individuals is associated with the immuno-suppressive cytokines transforming growth factor beta and EL-10. Higher levels of
the THi cytokines interferon gamma, tumour necrosis factor alpha and IL-2 seen in
lesional compared to non-lesional and healthy skin could be induced by subsequent
self-trauma and secondary infections. These results characterise the first spontaneously occurring animal model of human AD.