Immune regulation in atopic dermatitis

Curr Opin Immunol. 2000 Dec;12(6):641-6. doi: 10.1016/s0952-7915(00)00156-4.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Dermatitis, Atopic / immunology*
  • Humans
  • Lymphocyte Activation / immunology
  • Skin / immunology
  • T-Lymphocytes / immunology*