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Wataru Nishie

Researcher at Hokkaido University

Publications -  191
Citations -  4077

Wataru Nishie is an academic researcher from Hokkaido University. The author has contributed to research in topics: Bullous pemphigoid & Pemphigoid. The author has an hindex of 34, co-authored 186 publications receiving 3382 citations. Previous affiliations of Wataru Nishie include University of Freiburg & University Medical Center Freiburg.

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Humanization of autoantigen

TL;DR: It is shown that human autoimmune disease can be reproduced using genetically engineered model mice and injected human BP autoantibody into Col17-knockout mice rescued by the human ortholog, resulting in BP-like skin lesions and a human disease phenotype.
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Hair Follicle Stem Cells Provide a Functional Niche for Melanocyte Stem Cells

TL;DR: Collagen XVII (COL17A1/BP180/BPAG2), a hemidesmosomal transmembrane collagen, is highly expressed in hair follicle stem cells (HFSCs) and is required for the maintenance not only of HFSCs but also of melanocyte stem cells(MSCs), which do not express Col17a1 but directly adhere to HF SCs.
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Autoantibody Profile Differentiates between Inflammatory and Noninflammatory Bullous Pemphigoid

TL;DR: It is shown that the autoAb profile differentiates between inflammatory and noninflammatory BP, and that non inflammatory BP may be associated with dipeptidyl peptidase-IV inhibitors.
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Update on the pathogenesis of bullous pemphigoid: An autoantibody-mediated blistering disease targeting collagen XVII

TL;DR: This article summarizes the update on pathogenesis of BP, with a special focus on blister formation by autoAbs to COL17, and suggests other pathways, including a complement-independent pathway and a pathway involving IgE-autoAbs.
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Targeted skipping of a single exon harboring a premature termination codon mutation: implications and potential for gene correction therapy for selective dystrophic epidermolysis bullosa patients.

TL;DR: It is concluded that skipping of targeted exons using mutation-specific AON may show potential for future gene therapy for DEB patients, as it induced effective skipping of normal exon 70 containing 16 amino acids.