아토피피부염과 피부장벽
Atopic Dermatitis and Epidermal Barrier
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초록
Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disease in which genetic mutations and cutaneous hyperreactivity to environment stimuli play a role. The skin barrier is known to be damaged in patients with AD, both in acute eczematous lesions and in clinically unaffected skin. Skin barrier function can be impaired first by a genetic predisposition to produce increased levels of stratum corneum chymotryptic enzyme. This protease enzyme causes premature breakdown of corneodesmosomes, leading to damage of the epidermal barrier. The addition of environmental interactions can increase production of stratum corneum chymotryptic enzyme and impair epidermal barrier function. The epidermal barrier can also be damaged by exogenous proteases. One or more of these factors in combination might lead to a defective barriers, after then increasing the risk of allergen penetration and succeeding inflammatory reaction, thus contributing to exacerbations of this disease. The strong association between both genetic barrier defects and environmental factors to the barrier with AD suggests that epidermal barrier dysfunction is a primary event in the development of this disease. New concepts into the relation of the epidermal barrier function and its interaction with components of the innate and adaptive immune responses in patients with AD give rise to novel treatments.
Abstract
Atopic dermatitis (AD) is a multifactorial, chronic inflammatory skin disease in which genetic mutations and cutaneous hyperreactivity to environment stimuli play a role. The skin barrier is known to be damaged in patients with AD, both in acute eczematous lesions and in clinically unaffected skin. Skin barrier function can be impaired first by a genetic predisposition to produce increased levels of stratum corneum chymotryptic enzyme. This protease enzyme causes premature breakdown of corneodesmosomes, leading to damage of the epidermal barrier. The addition of environmental interactions can increase production of stratum corneum chymotryptic enzyme and impair epidermal barrier function. The epidermal barrier can also be damaged by exogenous proteases. One or more of these factors in combination might lead to a defective barriers, after then increasing the risk of allergen penetration and succeeding inflammatory reaction, thus contributing to exacerbations of this disease. The strong association between both genetic barrier defects and environmental factors to the barrier with AD suggests that epidermal barrier dysfunction is a primary event in the development of this disease. New concepts into the relation of the epidermal barrier function and its interaction with components of the innate and adaptive immune responses in patients with AD give rise to novel treatments.
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