IgA-binding structures in dermatitis herpetiformis skin are independent of elastic-microfibrillar bundles.
IgA-binding structures in dermatitis herpetiformis skin are independent of elastic-microfibrillar bundles.
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疱疹样皮炎皮肤中的 IgA 结合结构独立于弹性微原纤维束。
DOI：
10.1111/1523-1747.ep12515903
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Hall,RP
中科院分区：
文献类型：
--
作者：
Lightner,VA;Sakai,LY;Hall,RP
疱疹样皮炎（DH）的部分特征是在真皮-表皮交界处下方的乳头状真皮中存在伊加颗粒沉积。然而，伊加在DH皮肤中结合的结构的性质尚未得到明确证明。以前的免疫电镜研究使用过氧化物酶-抗过氧化物酶技术的结论是，伊加可能绑定到异常的弹性微纤维束。最近，已经开发了针对弹性微纤维束的主要组分的抗体，即抗纤维蛋白。此外，另一种真皮基质蛋白，hexabrachion，已被表征并发现在正常人皮肤中的分布类似于DH的伊加沉积物。利用抗体对hexabrachion，和人类伊加和免疫电镜与iminunogold染色技术，我们已经检查了皮肤从DH患者，以本地化伊加存款。5名DH患者的正常皮肤在真皮内显示出电子致密的斑块，这在正常受试者的皮肤中看不到。这些结构有时与基底膜区相邻，但表现为无定形，没有明确的纤维状结构。电子致密的补丁标记有抗人类伊加，但没有抗体的hexabrachion或hexabrachion。抗IgA抗体不标记正常基底膜。这些研究证实了DH患者皮肤中存在异常电子致密的无定形结构。由于这种缺乏与弹性微纤维束和缺乏标记的抗体对Escherin，我们建议，这些存款是不同的弹性组织的微纤维束，并可能代表伊加结合到降解的基底膜或孤立的皮肤IgA存款。
Dermatitis herpetiformis (DH) is characterized in part by the presence of granular deposits of IgA in the papillary dermis just beneath the dermal-epidermal junction. The nature of the structures to which IgA binds in DH skin, however, has not been clearly demonstrated. Previous immunoelectronmicroscopy studies using the peroxidase-antiperoxidase technique have concluded that the IgA may bind to abnormal elastic microfibrillar bundles. Recently, antibodies have been developed against a major component of the elastic microfibril bundles, fibrillin. In addition, another dermal matrix protein, hexabrachion, has been characterized and found in normal human skin in a distribution similar to the IgA deposits of DH. Utilizing antibodies against fibrillin, hexabrachion, and human IgA and immunoelectronmicroscopy with iminunogold staining techniques, we have examined the skin from patients with DH in order to localize the IgA deposits. Normal-appearing skin from five patients with DH exhibited electron-dense patches within the dermis, which were not seen in skin from normal subjects. These structures were sometimes adjacent to the basement membrane zone, but appeared amorphous and without a well-defined fibrillar structure. The electron-dense patches were labeled with anti-human IgA, but not with antibodies to fibrillin or hexabrachion. The anti-IgA antibody did not label the normal basement membrane. These studies confirm the presence of abnormal electron-dense, amorphous structures in the skin of patients with DH. Due to this lack of association with the elastic microfibril bundles and the lack of labeling with antibodies against fibrillin, we suggest that these deposits are distinct from the microfibrillar bundles of elastic tissue and may represent IgA bound to degraded basement membrane or isolated dermal deposits of IgA.