Vaccinia virus pathogenicity in atopic dermatitis is caused by allergen-induced immune response that prevents the antiviral cellular and humoral immunity.

Abstract

Atopic dermatitis (AD) serves as a contraindication for the immunization of AD patients with a live vaccinia virus (VV) vaccine. The antiallergen IgE interacts with the Fc receptors (FcepsilonRI) on dendritic cell (DC) membranes and with allergen molecules. The immunological events that lead to AD disease, the activation of the T-helper 2 (Th2) immune response, the synthesis of the cytokines IL-4, IL-5, IL-13, and the inhibition of the T-helper 1 (Th1) damage the capacity of the host to develop anti-VV cytotoxic cells (CTLs). In the presence of Th2-derived cytokine IL-4 in the AD skin and the synthesis of VV proteins that interfere recruitment of DCs by host cytokines, the VV can cause a generalized infection. Conceptually, new VV recombinants may be needed for human immunization. Such VV recombinants should lack the genes that interfere with the host immune system and express a mutated human IL-4 cytokine gene that will prevent negative regulatory mechanisms. Such improved VV recombinants may be used to express genes from pathogenic viruses.