这一阵子发贴回贴都不容易。大家这个时候还坚持讨论,更不容易哈!
新的研究表明,丝聚蛋白在过敏性湿疹中扮演重要角色。很多过敏性湿疹的患者有丝聚蛋白基因的突变。这些突变使得丝聚蛋白数量减少或缺失,造成表皮层渗漏。这时水分容易散失造成皮肤干燥,对过敏原的敏感性增加。
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Normal skin (above left): In the granular layer of normal skin, the large profilaggrin protein is dephosphorylated and enzymatically cut into 10-12 smaller filaggrin molecules (1). As these cells move up to form the stratum corneum, they flatten their shape by collapsing their keratin structure—a process aided by interaction with filaggrin proteins (2). In the stratum corneum, filaggrin degrades into amino acids essential for maintaining moisture in the outer layers of skin (3). The intact skin barrier of healthy skin keeps allergens, pathogens (bacteria and viruses) and chemical irritants out of the body (4).
Eczema (above right): Mutations in the filaggrin gene greatly reduce the amount of filaggrin protein in the skin or lead to its complete absence (1), resulting in cracks in the skin barrier(2) that expose the lower layers to allergens that are usually kept out, thus causing eczema(3). Once foreign material, such as an allergen, passes through the defective skin barrier, it is spotted by cells of the immune system, leading to inflammation of the skin and other allergic responses (4). If a child is exposed to allergens through the skin, that exposure is more likely to prime the immune system to react aggressively to that allergen later in life, explaining the coincidence of asthma and eczema seen in patients throughout the world.
英文链接: http://www.the-scientist.com/?articles.view/articleNo/29383/title/The-Allergy-Gene/