Immune regulation in atopic 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.
Akdis
C A
CA
Swiss Institute of Allergy and Asthma Research, Obere Strasse 22, CH-7270 Davos, Switzerland. akdisac@siaf.unizh.ch
Akdis
M
M
Trautmann
A
A
Blaser
K
K
D000818:Animals; D003876:Dermatitis, Atopic / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D012867:Skin / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*