Networks of single nucleotide polymorphisms of candidate genes to increase psoriasis risk.

本研究旨在探讨日本银屑病(寻常型银屑病200例，泛发性脓疱型银屑病10例，银屑病关节炎30例)发生发展的病理生理学特征。本研究的主要结果如下：第一，免疫学标志物(IL-12B、IL-36RN、肿瘤坏死因子-α、CTLA_4)和人类白细胞抗原可能参与了银屑病的发生发展。第二，IL-36RN基因缺陷是泛发性脓疱型银屑病发生的关键，而不是寻常型银屑病的发生。此外，IL-36RN的这些遗传缺陷是由于该基因的创始人效应造成的。第三，通过对FABP5基因敲除小鼠的实验，发现FABP5结合亚油酸在调节表皮细胞角蛋白基因K1方面非常重要。

The present study was to investigate the pathophysiological aspects concerning the development of psoriasis (psoriasis vulgaris (N=200), generalized pustular psoriasis(N=10), psoriatic arthritis(N=30) in Japan. We can summarize the results of the present study as follows: first, immunological markers (IL-12B, IL-36RN, TNF-α, and CTLA4) as well as HLA might be involved in the development of psoriasis. Second, genetic defects of the IL-36RN are essential to develop the generalized pustular psoriasis but not psoriasis vulgaris. Moreover these genetic defects of IL-36RN are due to the founder effect of the gene. Third, FABP5 combining linoleic acid is found to be very important in regulating cytokeratin gene K1 of the epidermis , by experiments using FABP5 knockout mice.