Immune regulation in atonic dermatitis

Atopic dermatitis is a chronic inflammatory skin disease with a pathogenesis of complex immune dysregulation and interplay of genetic, environmental and psychological factors. Activation and skin-selective homing of peripheral-blood T cells, and effector functions in the skin, represent sequential immunological events in the pathogenesis of atopic dermatitis. Both CD4(+) and CD8(+) T cells bearing the cutaneous-lymphocyte-associated antigen represent activated memory/effector T cell subsets and induce IgE, mainly via IL-13, and prolong eosinophil lifespan, mainly via IL-5. Dysregulated apoptosis in skin-homing T cells and keratinocytes contributes to the elicitation and progress of atopic dermatitis. T cell survival is enhanced in the skin by cytokines and extracellular matrix proteins, These activated T cells induce keratinocyte apoptosis, leading to eczema formation.