کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5649515 | 1407126 | 2017 | 34 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mouse Model of Hydroquinone Hypersensitivity via Innate and Acquired Immunity and its Promotion by Combined Reagents
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کلمات کلیدی
TNF2-hydroxyethyl methacrylateCHSLLNAMMASCIDeC3T helperTSLPnatural killer - (سلول های) کشنده طبیعیLocal lymph node assay - آزمایش گره لنفاوی محلیOxazolone - اگزازولونContact hypersensitivity - تماس با افزایش حساسیتtumor necrosis factor - فاکتور نکروز تومورThymic stromal lymphopoietin - لنفوپیتین استروما تیمیکMMA, Methyl methacrylate - متیل متا آکریلاتknockout - ناکاوتHEMA - هماHydroquinone - هیدروکینونsevere combined immunodeficient - کمبود ایمنی ترکیبی شدید
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We established a mouse model of contact hypersensitivity (CHS) to hydroquinone (HQ), a widespread chemical in our environment. HQ was painted onto flanks; then, HQ was challenged by painting onto ear pinnas on days 7 and 14. The CHS after the second challenge was markedly greater than that after the first challenge. Both challenges increased thymic stromal lymphopoietin and T helper type 2 cytokines in ear pinnas, whereas IFN-γ (typical T helper type 1 cytokine) was decreased, despite an increase in IL-18 (typical IFN-γ inducer). In nude mice (T cell-reduced), although a first challenge induced CHS, a second challenge did not augment it. In severe combined immunodeficient, severe combined immunodeficient-beige, and IL-1-deficient mice, CHS was not induced. However, CHS was inducible in severe combined immunodeficient-beige mice after transfer of natural killer cells from HQ-sensitized normal mice. Tretinoin (used for enhancing the skin-whitening effect of HQ) and resin monomers (used to prevent polymerization of HQ) lowered the HQ concentration needed to establish sensitization to HQ. The augmented CHS after a second challenge was reduced by JNJ7777120, dexamethasone, suplatast tosilate (T helper type 2-cytokine inhibitor), and anti-thymic stromal lymphopoietin antibody. These results suggest that (i) thymic stromal lymphopoietin, IL-1, and T and/or natural killer cells are important in establishing and augmenting CHS to HQ and (ii) inflammatory chemicals may promote CHS to HQ as adjuvants.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 137, Issue 5, May 2017, Pages 1082-1093
Journal: Journal of Investigative Dermatology - Volume 137, Issue 5, May 2017, Pages 1082-1093
نویسندگان
Kanan Bando, Yukinori Tanaka, Toshinobu Kuroishi, Keiichi Sasaki, Teruko Takano-Yamamoto, Shunji Sugawara, Yasuo Endo,