Increased susceptibility to cutaneous viral infections in atopic dermatitis: the roles of regulatory T cells and innate immune defects.

Much attention has been focused on the elucidation of mechanisms whereby atopic dermatitis (AD) skin lesions are especially susceptible to certain viral infections, such as herpes simplex virus (HSV). Although one of the most likely hypotheses is that the primary defect is in an impaired epidermal barrier function, alternative hypotheses include an imbalance between antiviral immune responses and regulatory T (T(reg)) cells, and the defects in the innate immune system. Eczema herpeticum (EH) occurs almost exclusively in patients with AD, particularly in those who fail to control skin inflammation. According to our scenario, expansions of T(reg) cells would be initially required for preventing such excessive inflammation resulting from the failure, and the expansions could in turn contribute to HSV reactivation, resulting in the initiation and progression of EH. A selective impairment of Toll-like-receptor-2-mediated proinflammatory cytokine production by monocytes could be the additional mechanism responsible for the increased susceptibility of AD subjects to curtain viral infections. Here we provide several potential explanations for why AD patients are at greater risk for eczema molluscatum.