Abstract
Atopic dermatitis (AD) is a recurrent chronic eczematous skin disease. Histoclogically AD shows a large number of T cells, eosinophils and mast cells infiltration into the lesional skin. Recently, chemokines are identified. Specific chemokines attract specific types of leukocytes in the inflammatory sites. TARC/CCL17, MDC/CCL22, CTACK/CCL27 participate in the pathogenesis of AD. High levels of serum CCL17 and CCL27 have been identified in AD patients, in accordance with the strong expression of these molecules in the lesional epidermis of AD patients. Corticosteroids and tacrolimus inhibit these productions in PBMCs of AD patients. TSLP, secreted by epidermal kertatinocytes, induce CCL17 and CCL22 mRNA expression in lesional skin in K14/TSLP transgenic mice. Future therapies targeting chemokines and chemokine receptors will be discussed.
