Abstract
The term atopic dermatitis (AD) is commonly used in cats. At present, however, there is little known about the pathogenesis of feline AD.
The aim was to investigate various aspects of the immunopathogenesis in a defined group of cats with signs and symptoms of atopic dermatitis and compare our findings with
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the immunoregulation of atopic dermatitis in humans.
The presence of antigen-specific IgE in serum of AD cats was investigated by means of the Prausnitz-Küstner (PK) test and the passive cutaneous anaphylaxis test (PCA). Positive reactions in the PCA-test and PK-test were observed with both heated sera and unheated sera. These results indicate that heat-stabile cytophilic antibodies, as well as heat-labile antibodies may be involved.
The occurrence of Langerhans cells (LC) was investigated. Significantly higher numbers of CD1a+ cells and MHC class II+ cells were observed in the epidermis and dermis of AD cats. Immunofluorescence-double labeling revealed staining of CD1a+ cells with MHC class II antibody. In some LC the typical tennis-racket-shaped Birbeck granules were observed with electronmicroscopy.
In the dermis of lesional and nonlesional skin of AD cats a significantly higher number of CD3+ T cells, with a predominance of CD4+ T cells, was observed in lesional and nonlesional skin. In skin of healthy control animals only few CD4+ T cells were observed. The CD4+/CD8+ cell ratio in peripheral blood did not differ significantly between AD cats and control cats.
IL-4+ cells were found in the epidermis in lesional skin only and in the superficial dermis, in both lesional and nonlesional skin. Very few IL-4+ cells were present in the dermis of the control animals. The IL-4+ cells co-stained with antibodies against CD4 and a pan-T cell whilst double-labeling of IL-4 and mast cell chymase was observed in only a few cells. Cross-reactivity of the antibody against human IL-4 with feline IL-4 was confirmed by Western blotting with recombinant fIL-4.
Mast cells (MC) and eosinophils were quantified and MC were characterized according to their protease content, i.e. chymase and tryptase. In both healthy cats and cats with AD, the MC counts varied considerably, albeit in the diseased cats at a significantly higher level than in the healthy cats. Eosinophils were exclusively found in cats with atopic dermatitis. In lesional and nonlesional skin a significantly lower number of tryptase-containing MC were found in comparison with chymase- containing MC. A significant difference in the number of tryptase-positive MC in lesional and nonlesional skin of AD cats was not observed.
Atopy patch testing (APT) was adapted for cats. Erythematous skin reactions were observed after 24-hours in 1 cat and after 48-hours in 3 cats (n=6) with AD. No reactions were seen at the negative control sites of atopic cats nor did any of the healthy control cats display positive APT reactions.
The cellular infiltrate in the skin of biopsy sites at 24 hours after APT revealed significantly increased numbers of IL-4+, CD4+, CD3+, MHC class II+ and CD1a+ cells in one AD cat with visually positive patch test reactions. All AD cats (except one) had significantly increased IL-4+ T cell numbers at 24 and /or 48 hours APT sites.
In summary, these findings suggest that the immunopathogenesis of atopic dermatitis in cats may be comparable to that in humans. However, in view of the current knowledge, it might be more prudent to call this entity "feline atopy-like dermatitis"
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