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Atopic dermatitis is a heritable disorder in which animals are hypersenstive to common environmental allergens. It is one of the most common skin diseases of dogs worldwide.

Atopic dermatitis is a heritable disorder in which animals are hypersenstive to common environmental allergens. It is one of the most common skin diseases of dogs worldwide.

The most common allergens involved in atopic dermatitis are those of house dust mites (''Dermatophagoides farinae'') and grain mites. Human and animal danders, house dust, grass and tree pollen and moulds also frequently incite reactions. Susceptible animals produce allergen-specific IgE to normally-innocuous environmental allergens. This IgE then binds to receptors on cutaneous mast cells to facilitate degranulation on further allergen exposure¹. It is thought that allergen exposure occures via percutaneous absoprtion. Degranulation of mast cells in response to allergen-specific IgE is a type 1 (immediate) hypersensitivity reaction, which results in the release of histamine, cytokines, chemokines, and other chemical mediators. The cytokines involved are biased towards a Th2-type response, with particularly high production of IL-4. IL-4 is a key cytokine for further production of IgE by B-cells. . bacterial superantigens, autoantigens release via keratinocyte samage plays a role in perpetuating inflammation.

The most common allergens involved in atopic dermatitis are those of house dust mites (''Dermatophagoides farinae'') and grain mites. Human and animal danders, house dust, grass and tree pollen and moulds also frequently incite reactions. Susceptible animals produce allergen-specific IgE to these normally-innocuous allergens, which then binds to receptors on cutaneous mast cells. Atopic animals may have defects in the epidermis, leading to impaired barrier function, and it is thought that further allergen exposure occures via percutaneous absorption. This further exposure gives mast cell degranluation, releasing istamine, cytokines, chemokines, leukotrienes, prostaglandins and other chemical mediators. This is a type 1 (immediate) hypersensitivity reaction¹, and leads to vasodilation, inflammatory cell infiltration and pruritus. It appears that the cytokines involved are abnormally biased towards a Th2 response. IL-4 in particular is produced; this cytokine is responsible for B-cell production of IgE. Bacterial superantigens and autoantigens released due to keratinocyte damage play a role in perpetuating inflammation.

==Signalment==

==Signalment==