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Abnormal epidermal barrier in the pathogenesis of psoriasis

机译：银屑病发病机制中的表皮屏障异常

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Almost 2 decades ago, Williams and Elias suggested a unifying concept for the pathogenesis of disorders of cornification, according to which the integrity of the epidermal barrier and its effective function is an important factor in the regulation of epidermal DNA synthesis. Interference with the barrier integrity or function will result in epidermal hyperplasia and may be the primary event leading to hyperproliferative skin diseases, such as psoriasis.We have analyzed alterations to several structures of the epidermal barrier that might be responsible for barrier dysfunction and thus lead to hyperproliferation of the epidermis in an attempt to repair the barrier and, as a result, might be inducers of psoriasis. There are several convincing reports indicating that inhibiting of epidermal transglutaminase may lead to epidermal hyperproliferation and that this stimulus might trigger psoriasis among genetically predisposed patients.Disturbance of epidermal barrier function caused by derangement of lipid or cholesterol or ceramide synthesis leads to increased DNA synthesis and epidermal hyperplasia and as a result might be an inducer of psoriasis. We could find little evidence to show that defective defense of the epidermis or an abnormal response of it to bacteria plays a role in the pathogenesis of psoriasis.Accumulating data indicate that there is an association of psoriasis and mutations of genes within the epidermal differentiation complex, which are crucial for the development, maturation, cornification, cross-linking, and terminal differentiation of the epidermis, called psoriasis susceptibility locus 4.
机译：大约2十年前，Williams和Elias提出了一个统一的概念，用于认识角化疾病的发病机理，根据这一概念，表皮屏障的完整性及其有效功能是调节表皮DNA合成的重要因素。干扰屏障的完整性或功能将导致表皮增生，并且可能是导致过度增生性皮肤疾病（如牛皮癣）的主要事件。我们分析了表皮屏障的几种结构变化，这些结构可能导致屏障功能障碍，从而导致表皮过度增生，试图修复该屏障，因此可能是牛皮癣的诱因。有一些令人信服的报道表明，抑制表皮转谷氨酰胺酶可能导致表皮过度增殖，并且这种刺激可能会触发遗传易感患者中的牛皮癣。由于脂质或胆固醇紊乱或神经酰胺合成引起的表皮屏障功能障碍导致DNA合成和表皮增加增生，因此可能是牛皮癣的诱因。我们几乎找不到证据表明表皮防御能力不足或对细菌的异常反应在牛皮癣的发病机理中起作用。大量数据表明，牛皮癣与表皮分化复合物中的基因突变有关，这些对表皮的发育，成熟，角质化，交联和终末分化至关重要，这被称为牛皮癣易感性基因座4。

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