کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6075045 | 1203492 | 2016 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Influence of Th2 Cytokines on the Cornified Envelope, Tight Junction Proteins, and β-Defensins in Filaggrin-Deficient Skin Equivalents
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کلمات کلیدی
AMPT helper type 1human β-defensin 2hBD-1hBD-3T helper type 2Human β-defensin 3HBD-2FLGTh2Th1TSLPTight junction - اتصال تنگtumor necrosis factor-α - تومور نکروز عامل αAtopic dermatitis - درماتیت آتوپیکTNF-α - فاکتور نکروز توموری آلفاfilaggrin - فیلهگرینThymic stromal lymphopoietin - لنفوپیتین استروما تیمیکAntimicrobial peptide - پپتیدهای ضدمیکروبی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Influence of Th2 Cytokines on the Cornified Envelope, Tight Junction Proteins, and β-Defensins in Filaggrin-Deficient Skin Equivalents Influence of Th2 Cytokines on the Cornified Envelope, Tight Junction Proteins, and β-Defensins in Filaggrin-Deficient Skin Equivalents](/preview/png/6075045.png)
چکیده انگلیسی
Atopic dermatitis is a chronic skin condition with complex etiology. It is characterized by skin barrier defects and T helper type 2 (Th2)-polarized inflammation. Although mutations in the filaggrin gene are known to be prominent genetic risk factors for the development of atopic dermatitis, the interdependency between these and an altered cytokine milieu is not fully understood. In this study, we evaluated the direct effects of filaggrin deficiency on the cornified envelope, tight junction proteins, and innate immune response, and report the effects of Th2 cytokines in normal and filaggrin-deficient skin equivalents. Supplementation with IL-4 and IL-13 led to distinct histologic changes and significantly increased skin surface pH, both of which were enhanced in filaggrin knockdown skin equivalents. We detected a compensatory up-regulation of involucrin and occludin in filaggrin-deficient skin that was dramatically disturbed when simultaneous inflammation occurred. Furthermore, we found that a lack of filaggrin triggered an up-regulation of human β-defensin 2 via an unknown mechanism, which was abolished by Th2 cytokine supplementation. Taken together, these results indicate that defects in the epidermal barrier, skin permeability, and cutaneous innate immune response are not primarily linked to filaggrin deficiency but are rather secondarily induced by Th2 inflammation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 136, Issue 3, March 2016, Pages 631-639
Journal: Journal of Investigative Dermatology - Volume 136, Issue 3, March 2016, Pages 631-639
نویسندگان
Stefan Hönzke, Leonie Wallmeyer, Anja Ostrowski, Moritz Radbruch, Lars Mundhenk, Monika Schäfer-Korting, Sarah Hedtrich,