Atopic dermatitis may be a genetically determined dysmaturation of ectodermal tissue, resulting in disturbed T-lymphocyte maturation. A hypothesis.

Abstract

Although atopic dermatitis is a skin disorder, it includes immune deviations such as T-cell accumulation and activation in the skin, resulting in chronic, relapsing eczema. The T-lymphocyte activation in the skin is not accompanied by specific allergies in up to two thirds of the patients. It has been shown that T-cell lines and clones can be established from skin biopsies of patients with atopic dermatitis showing cytokine-dependent, but antigen-independent, continuous growth in vitro. This indicates the existence of skin-homing T-lymphocytes with growth requirements different from those of mature T-lymphocytes in the blood. We suggest that atopic dermatitis is a genetically determined change of ectodermal tissue. The thymic epithelium is derived from the ectoderm, and because of that we hypothesize that the maturation of the T-cell immune system of persons who develop atopic dermatitis is disturbed due to a faulty selection of T-lymphocytes in the thymus. "Dys"-matured T-cells leave the thymus as a consequence of faulty selection and continue their growth in the skin. The cells are eventually eradicated by the immune surveillance conducted by the normal part of the patients' immune system and as a consequence of diminished output of faulty selected T-lymphocytes during maturation. Because of the increased proliferation capacity of the aberrant T-cells, a cytokine imbalance occurs and in some patients this leads to the development of type I allergies due to a skewing of the humoral immune system towards IgE production.