Hokkaido University · 의학
히데유키 우지에 교수의 연구실은 주로 자가면역성 브러저성 피부질환, 특히 브러저 페프기드(Bullous Pemphigoid)를 중심으로 한 면역병리학적 기전을 규명하는 데 중점을 두고 있습니다. 인간의 타입 XVII 콜라겐(COL17)을 인간 유전자로 보유한 마우스 모델을 개발하여, 자가항체에 의한 브러저 형성 메커니즘과 보조인자인 보체 경로의 기여 여부를 정밀하게 분석하고 있습니다. 또한 보체 의존적이지 않은 신경전달 경로의 역할 등, 기존 이론을 넘어서는 새로운 병태생리학적 메커니즘 탐색을 지속하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
An estimated 20-25% of the population is affected by chronic, non-communicable inflammatory skin diseases. Chronic skin inflammation has many causes. Among the most frequent chronic inflammatory skin diseases are atopic dermatitis, psoriasis, urticaria, lichen planus, and hidradenitis suppurativa, driven by a complex interplay of genetics and environmental factors. Autoimmunity is another important cause of chronic skin inflammation. The autoimmune response may be mainly T cell driven, such as i
Complement activation and subsequent recruitment of inflammatory cells at the dermal/epidermal junction are thought to be essential for blister formation in bullous pemphigoid (BP), an autoimmune blistering disease induced by autoantibodies against type XVII collagen (COL17); however, this theory does not fully explain the pathological features of BP. Recently, the involvement of complement-independent pathways has been proposed. To directly address the question of the necessity of the complemen
Abstract The pemphigoid group is a category of autoimmune subepidermal blistering diseases in which autoantibodies deposit linearly at the epidermal basement membrane zone ( BMZ ). The main subtypes of pemphigoid mediated by immunoglobulin G autoantibodies are bullous pemphigoid ( BP ), mucous membrane pemphigoid ( MMP ) and epidermolysis bullosa acquisita ( EBA ). To establish the first guidelines approved by the Japanese Dermatological Association for the management of pemphigoid diseases, the
Bullous pemphigoid (BP), the most common autoimmune blistering disease, is caused by autoantibodies against type XVII collagen (COL17). To establish an active stable BP animal model that demonstrates the persistent inflammatory skin lesions initiated by the anti-human COL17 Abs, we used COL17-humanized (COL17(m-/-,h+)) mice that we recently produced. First, we generated immunodeficient Rag-2(-/-)/COL17-humanized mice by crossing Rag-2(-/-) mice with COL17-humanized mice. Then, splenocytes from w
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Bullous pemphigoid (BP) is the most common autoimmune blistering disease. BP patients have autoantibodies against type XVII collagen (COL17, also called BP180 or BPAG2), a type II transmembrane protein that spans the lamina lucida and projects into the lamina densa of the epidermal basement membrane. The non-collagenous 16A domain of COL17 is considered to contain pathogenic epitopes of BP. The transfer of immunoglobulin (Ig)G from BP patients fails to cause blisters on mouse skin probably due t
Bullous pemphigoid (BP) is a subepidermal blistering disease induced by autoantibodies to type XVII collagen (COL17, also called BP180) and BP230. Previous studies using patients' samples and animal disease models elucidated the complement-dependent and complement-independent pathways of blister formation, the pathogenic roles of immune cells (T and B cells, macrophages, mast cells, neutrophils, eosinophils), and the pathogenicity of IgE autoantibodies in BP. This review introduces the recent pr
Pyoderma gangrenosum (PG) is a neutrophilic dermatosis characterized by destructive, necrotizing and noninfective ulceration of the skin mostly on lower extremities. PG is well known as a complication of Takayasu's arteritis in Japan. However, this association is not commonly observed in North American and European patients. We describe a case of PG that was associated with Takayasu's arteritis who was successfully treated with systemic cyclosporin. We have reviewed 35 well-documented PG cases w
This paper reports a unique case of coexistence of vitiligo vulgaris, lichen planus and psoriasis vulgaris in a 53-year-old man. Five years after the onset of vitiligo, lichen planus developed on his lower lip. Another 4 years after the onset of lichen planus, he also exhibited psoriasis on his upper arms and trunk. Both the lichen planus and psoriasis occurred on lesions of the preceding vitiligo vulgaris. We discuss potential mechanisms for association of these three dermatoses, including Koeb
