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银屑病的发病机制与遗传学

Pathogenesis and genetics of psoriasis.

作者信息

Menter A

机构信息

Division of Dermatology, Baylor University Medical Center, Dallas, Texas, USA.

出版信息

Cutis. 1998 Feb;61(2 Suppl):8-10.

PMID:9787986
Abstract

Our ever-expanding knowledge of the pathogenesis of psoriasis has finally matched that of other genetically based autoimmune diseases. No longer simply considered a disease of the skin, psoriasis is now widely recognized as a hereditary-based, systemic disease with cutaneous manifestations. The pathogenesis of psoriasis involves both genetic predisposition and T cell-dependent mechanisms. Population, family, and twin studies all strongly suggest an important genetic component, coupled with an environmental trigger, in the pathogenesis of psoriasis. Furthermore, genetic-linkage studies have found multiple genetic loci for psoriasis. The autoimmune component of psoriasis is substantiated by multiple findings, including the isolation of activated T cells within the lesions. Our current therapies for psoriasis are not target-specific. As we further unravel the genetic basis for psoriasis, treatments will improve together with the exciting potential for gene therapy in the future.

摘要

我们对银屑病发病机制的认识不断扩展,终于与其他基于遗传的自身免疫性疾病相匹配。银屑病不再仅仅被视为一种皮肤病,现在它被广泛认为是一种具有皮肤表现的基于遗传的全身性疾病。银屑病的发病机制涉及遗传易感性和T细胞依赖性机制。人群、家族和双胞胎研究均有力地表明,在银屑病的发病机制中,重要的遗传因素与环境触发因素相互作用。此外,基因连锁研究已经发现了多个银屑病相关的基因位点。银屑病的自身免疫成分有多项研究结果证实,包括在皮损内分离出活化的T细胞。我们目前治疗银屑病的方法并非靶向特异性的。随着我们进一步揭示银屑病的遗传基础,治疗方法将会得到改进,未来基因治疗也具有令人兴奋的潜力。

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