Basis for the barrier abnormality in atopic dermatitis: Outside-inside-outside pathogenic mechanisms

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY

卷:121

Review

Elias, Peter M.³  Hatano, Yutaka^1,3  Williams, Mary L.^1,2 

[1] Univ Calif San Francisco, Dept Dermatol, San Francisco, CA 94143 USA

[2] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA

[3] Vet Affairs Med Ctr, Dermatol Serv, San Francisco, CA 94121 USA

关键词: antimicrobial peptides;    atopic dermatitis;    barrier function;    barrier repair;    cytokines;    filaggrin;    pH;    psychologic stress;    Staphylococcus aureus;    serine proteases;    T(H)2 cells;   

DOI  :  10.1016/j.jaci.2008.01.022

来源: Elsevier

【 摘 要 】

Until quite recently, the pathogenesis of atopic dermatitis (AD) has been attributed to primary abnormalities of the immune system. Intensive study revealed the key roles played by T(H)1/T(H)2 cell dysregulation, IgE production, mast cell hyperactivity, and dendritic cell signaling in the evolution of the chronic, pruritic, inflammatory dermatosis that characterizes AD. Accordingly, current therapy has been largely directed toward ameliorating T(H)2-mediated inflammation and pruritus. In this review we will assess emerging evidence that inflammation in AD results from inherited and acquired insults to the barrier and the therapeutic implications of this paradigm.

【 授权许可】

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