ABSTRACT
Contact dermatitis (CD), an infl ammatory response in the skin due to external stimuli, is a complex phenomenon involving epidermal cells, fi broblasts, and endothelial cells as well as invading leukocytes interacting under the control of a network of cytokines and lipid mediators [1,2]. Traditionally divided into irritant and allergic mechanisms, the former results from toxic irritant chemicals and the latter represents a delayedtype hypersensitivity reaction [3]. Irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) share similar cellular and molecular pathways to achieve the same compensatory outcome, the reestablishment of dermal homeostasis [4].
