کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5649816 | 1407134 | 2017 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Research Techniques Made Simple: Mouse Models of Autoimmune Blistering Diseases
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کلمات کلیدی
EBADermatitis herpetiformisAutoimmune blistering diseaseepidermolysis bullosa acquisita - اپیدرمولیز گوشتی آیسیتاMHC - مجموعه سازگاری بافتی اصلیmajor histocompatibility complex - مجموعه سازگاری بافتی اصلیtype XVII collagen - نوع XVII کلاژنtype VII collagen - نوع کلاژن VIIbullous pemphigoid - پمفیگوئه گوسفندpemphigus vulgaris - پمفیگوس ولگاریس
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Autoimmune blistering diseases are examples of autoantibody-mediated, organ-specific autoimmune disorders. Based on a genetic susceptibility, such as a strong HLA-class II association, as yet unknown triggering factors induce the formation of circulating and tissue-bound autoantibodies that are mainly directed against adhesion structures of the skin and mucous membranes. Compared with other autoimmune diseases, especially systemic disorders, the pathogenicity of autoimmune blistering diseases is relatively well described. Several animal models of autoimmune blistering diseases have been established that helped to uncover the immunological and molecular mechanisms underlying the blistering phenotypes. Each in vivo model focuses on specific aspects of the autoimmune cascade, from loss of immunological tolerance on the level of T and B cells to the pathogenic effects of autoantibodies upon binding to their target autoantigen. We discuss current mouse models of autoimmune blistering diseases, including models of pemphigus vulgaris, bullous pemphigoid, epidermolysis bullosa acquisita, and dermatitis herpetiformis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 137, Issue 1, January 2017, Pages e1-e6
Journal: Journal of Investigative Dermatology - Volume 137, Issue 1, January 2017, Pages e1-e6
نویسندگان
Robert Pollmann, Rüdiger Eming,