Canine atopic dermatitis (AD) is a pruritic (unpleasant sensation that provokes the desire to scratch) skin disease that holds a complex pathogenesis.  It results from a combination of immune system dysfunction, compromised skin barrier, and genetic predisposition to environmental allergen oversensitivity. Dogs with this disease suffer from constant skin irritation and experience daily discomfort. Medicinal treatment is beneficial for symptom relief, however allergen specific immunotherapy has provided good clinical results.

Due to their anti-inflammatory and immune modulation properties, mesenchymal stem cells may act as a beneficial treatment for atopic dermatitis. Recent insights in genetics and pathophysiology of AD point to the role of structural abnormalities and immune dysregulation in the skin. The skin’s layers are the first line of defense against pathogens, allergens, or any other agents in the environment. Patients with AD have a unique predisposition to elevated levels of these types of irritants that penetrate the dermal layers of the skin and trigger immune responses.

Another driver of AD is immune system dysfunction. The normal regulation of inflammatory allergic responses is a balance between Th1 and Th2 cells over the control of allergy triggers. The mechanism for allergic responses is based on the secretions of Th1 (non-allergenic) cytokines, such as Il-2 and INF-g, and Th2 (pro-allergenic) cytokines, such as IL-4, IL-5 and IL-13. Further, active Th1 cells result in B cells to secrete IgG. Active Th2 cells result in the differentiation of B cells into plasma cells, which secrete IgE. Ultimately, IgE stimulates inflammation, pushing cells into an allergenic pathway. Theory states that there is equilibrium between the IgG and IgE, which modulates tolerance. The dysfunction of this equilibrium, coupled with over-exposure due to a compromised skin barrier, is the root cause of AD.

Mesenchymal stem cells, immune-modulatory activity performers, are being researched regarding their role in modulating AD. Recently, the MSC functions of suppression for T- and B-cell proliferation have been heavily researched. The therapeutic effects of MSCs on AD, a Th2-dominant disease, however, have not. If MSCs are found to inhibit the pathophysiology by decreasing Th2 cell activations and infiltration in skin lesions and reducing serum levels of IgE, a major criterion for the benefit of AD treatment would be met. Ultimately, the major goal is to help patients gain relief from chronic pruritus and to eliminate the amount of constant scratching.