¹Departments of Pediatrics and the HB Wells Center for Pediatric Research, Indianapolis-Indiana, United States of America
²Departments of Pediatrics and the HB Wells Center for Pediatric Research, Indianapolis- Indiana, United States of America.
³Departments of Pediatrics, Indianapolis-Indiana, United State of America.
⁴Department of Dermatology, Indianapolis-Indiana, United State of America
⁵Departments of Pediatrics and the HB Wells Center for Pediatric Research, Indianapolis-Indiana, United States of America.
⁶M.D., Ph.D. HB Wells Center for Pediatric Research, and the Department of Dermatology, and the Richard L. Roudebush V. A. Medical Center, Indiana University School of Medicine, Indianapolis – Indiana, United States of America.

Recebido em 07.12.07. Aprovado pelo Conselho Consultivo e aceito para publicação em 09.01.2008. * Work done at: H. B Wells Center for Pediatric Research, James Whitcomb Riley Hospital for Children - Indiana University School of Medicine, Indianapolis - Indiana, United States of America. Conflict of interest / Conflito de interesse: None Financial funding / Suporte financeiro: This manuscript was supported in part by grants from the Riley Memorial Association, and the United States of America National Institutes of Health grants HL62996, U19 AI070448 and Veteran’s Administration Merit Award. How to cite this article / Como citar este artigo: Sehra S, Barbé-Tuana FM, Holbreich M, Mousdicas N, Kaplan MH, Travers JB. Clinical correlations of recent developments in the pathogenesis of atopic dermatitis. An Bras Dermatol. 2008;83(1):57-73. How to cite this article / Como citar este artigo: Kahawita IP, Walker SL, Lockwood DNJ. Leprosy type 1 reactions and erythema nodosum leprosum. An Bras Dermatol. 2008;83(1):75-82.

Correspondência:
Jeffrey B. Travers H. B Wells Center for Pediatric Research James Whitcomb Riley Hospital for Children Rm 2659 Indiana University School of Medicine 702 Barnhill Drive Indianapolis, IN 46202 Fax: 317 274-5378 "email":jtravers@iupui.edu

 

Resumo

Atopic dermatitis is a chronic inflammatory skin disease with a steadily increasing prevalence affecting 10-20 % of infants and 1-3% of adults globally. It is often the first clinical manifestation of atopic disease preceding asthma and allergic rhinitis. Probably half of the children with atopic dermatitis develop some other form of atopic disease later in life. The pathogenesis involves a complex interplay of factors including genetic predisposition due to altered immune or skin barrier function, interactions with the environment such as food and allergen exposures, and infectious triggers of inflammation. In this review, we summarize the recent advances in understanding the contribution of different factors in the pathophysiology of atopic dermatitis and how insights provide new therapeutic potential for its treatment.

Palavras-chave: EOSINÓFILOS, ASTHMA, ATOPIC DERMATITIS, ECZEMA, EOSINOPHILS, GENETICS, IMMUNOGLOBULIN E, KERATINOCYTES, ASMA, CERATINÓCITOS, ECZEMA, GENÉTICA, IMUNOGLOBULINA E, LINFÓCITOS T, RINITE, DERMATITE ATÓPICA

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