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Pathogenesis of Atopic Dermatitis: Current Paradigm | ||
| Iranian Journal of Immunology | ||
| مقاله 1، دوره 16، شماره 2، شهریور 2019، صفحه 97-107 اصل مقاله (541 K) | ||
| نوع مقاله: Review Article | ||
| شناسه دیجیتال (DOI): 10.22034/iji.2019.80253 | ||
| نویسندگان | ||
| Masutaka Furue* ؛ Dugarmaa Ulzii؛ Yen Vu؛ Gaku Tsuji؛ Makiko Kido-Nakahara؛ Takeshi Nakahara | ||
| Department of Dermatology, Faculty of Medical Sciences, Kyushu University, Japan | ||
| چکیده | ||
| Atopic dermatitis (AD) is characterized by skin inflammation, barrier dysfunction and chronic pruritus. In this review, recent advances in the pathogenesis of AD are summarized. Clinical efficacy of the anti-IL-4 receptor antibody dupilumab implies that type 2 cytokines IL-4 and IL-13 have pivotal roles in atopic inflammation. The expression of IL-4 and IL-13 as well as type 2 chemokines such as CCL17, CCL22 and CCL26 is increased in the lesional skin of AD. In addition, IL-4 and IL-13 down-regulate the expression of filaggrin in keratinocytes and exacerbate epidermal barrier dysfunction. Keratinocytes in barrier-disrupted epidermis produce large amounts of thymic stromal lymphopoietin, IL-25 and IL-33, conducing to type 2 immune deviation via OX40L/OX40 signaling. IL-31, produced by type 2 T cells, is a cardinal pruritogenic cytokine. IL-4 and IL-13 also amplify the IL-31-mediated sensory nerve signal. These molecules are particularly important targets for future drug development for AD. | ||
| کلیدواژه‌ها | ||
| Atopic Dermatitis؛ IL-4؛ IL-13؛ IL-31؛ OX40 | ||
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آمار تعداد مشاهده مقاله: 9,589 تعداد دریافت فایل اصل مقاله: 6,531 |
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