Immune regulation in atonic dermatitis

Atopic dermatitis is a chronic inflammatory skin disease with a pathogenesi s of complex immune dysregulation and interplay of genetic, environmental a nd psychological factors. Activation and skin-selective homing of periphera l-blood T cells, and effector functions in the skin, represent sequential i mmunological events in the pathogenesis of atopic dermatitis. Both CD4(+) a nd CD8(+) T cells bearing the cutaneous-lymphocyte-associated antigen repre sent activated memory/effector T cell subsets and induce IgE, mainly via IL -13, and prolong eosinophil lifespan, mainly via IL-5. Dysregulated apoptos is 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 ind uce keratinocyte apoptosis, leading to eczema formation.