Atopic dermatitis used to be defined as a type 1 hypersensitivity with production of IgE specific for airborne allergens. This mast cell-bound IgE was supposed to be cross-linked by inhaled airborne allergens. Cross-linking leads to mast cell degranulation with release of inflammatory mediators and subsequent clinical signs. Today, most dermatologists and allergists agree that although inhaled allergens may be responsible for allergic rhinitis and allergic asthma, atopic dermatitis is triggered by percutaneous absorption of allergens which explains most of the predilection sites in the dog, i.e., interdigital, axillary, ventral and facial dermatitis.

Allergen-specific IgE has been demonstrated on the surface of Langerhans cells, providing a link between delayed type hypersensitivity and atopic dermatitis. Development of clinical signs may or may not occur with increased allergen-specific IgE concentrations, IgE may not be central to the pathogenesis of atopic dermatitis. T cell reactivity and cytokine release in patients with atopic dermatitis differ from normal individuals and normalize after successful immunotherapy, pointing to the central role of T cells in the disease. In humans, atopic dermatitis may be caused by percutaneously absorbed airborne allergens, but also by ingested food allergens and as food reactions in the dog and cat are clinically indistinguishable from nonseasonal atopic dermatitis, we may consider adverse food reaction a part of atopic dermatitis rather than a completely separate entity.

Research into the pathogenesis of atopic dermatitis has also helped explain our problems with various treatment modalities and develop new treatment options. Glucocorticoids have long been the predominant drug used for the treatment of atopic dermatitis. Due to their frequent side effects, particularly in dogs and humans, and increased public awareness of these adverse effects, owners increasingly requests alternatives. Antihistamines and fatty acids have been advocated as therapeutic agents in atopic dermatitis, but their success rate particularly in the dog is fairly low. Recent studies have provided evidence, that neither inflammatory leukotrienes (whose production is competitively inhibited by fatty acid supplementation) nor histamine (whose receptors are blocked by antihistamines) are important mediators of pruritus in the dog, explaining the low success rate. In addition, the optimal dose and ratio of omega 3 and 6 fatty acids are subject to much ongoing research and by no means clearly established. Although the mechanism of action of allergen-specific immunotherapy is not clear, “allergy shots” have been shown in humans to normalize T cell reactivity, studies are ongoing to confirm this in dogs. Rush immunotherapy (where the normal induction period of weeks to months is abbreviated to a few hours) has recently been introduced into veterinary dermatology and shown to be a feasible alternative to conventional immunotherapy. Studies are ongoing to evaluate if rush immunotherapy has a higher success rate or a quicker response than conventional allergy shots. A new drug recently introduced for the treatment of atopic dermatitis in humans and animals is cyclosporine. Cyclosporine inhibits the release of interleukin 2, the cytokine predominantly responsible for T cell activation. Several studies have evaluated this drug in atopic humans and dogs and results have been very encouraging, further emphasizing the central role of T-cells in atopic dermatitis. Further treatment options currently evaluated in humans are anti-IL-4 and anti-IL5 antibodies changing the T helper 2 cytokine profile seen in early atopic dermatitis and modified allergen-specific immunotherapies with greatly enhanced immunogenicity, but greatly diminished allergenicity.