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银屑病中的细胞表面碳水化合物。凝集素染色提示携带岩藻糖残基的糖缀合物存在细胞质转运缺陷。

Cell surface carbohydrates in psoriasis. Defective cytoplasmic transport by glycoconjugates carrying fucose residues suggested by lectin staining.

作者信息

Schaumburg-Lever G, Alroy J, Ucci A, Lever W F, Orfanos C E

出版信息

J Am Acad Dermatol. 1984 Dec;11(6):1087-94. doi: 10.1016/s0190-9622(84)70264-7.

Abstract

Eleven biopsy specimens of normal skin and twenty-four biopsy specimens of psoriatic lesions were examined histochemically by using several lectins (Ulex europaeus, UEA-1; Dolichos biflorus, DBA; Bandeirea simplicifolia, BS-I; Concanvalia ensiformis, Con A; Triticum vulgaris, WGA; Ricinus communis, RCA; Arachis hypogoea, PNA) in order to evaluate the presence and distribution of various carbohydrates in normal and psoriatic keratinocytes. The findings revealed that keratinocytes from psoriatic lesions are distinguished by a different composition of carbohydrate residues incorporated in their plasma membranes. In particular, the intracellular transport of alpha-L-fucose, alpha-D-mannose, and alpha-D-glucose to the plasma cell membrane is impeded, whereas their synthesis in the cytoplasm of the psoriatic keratinocytes is largely unaltered. In addition, due to the lack of terminal alpha-L-fucose, the alpha-D-N-acetyl-galactosamine and alpha-D-galactose residues cannot be transferred to the plasma membranes and, therefore, the antigens for blood groups A and B remain incomplete in psoriatic epidermis. On the basis of these findings and in comparison with previous findings of our group on hyperproliferative, malignant keratinocytes, it is concluded that particularly the disordered cytoplasmic transport of alpha-L-fucose-carrying glycoconjugates may represent a specific defect in psoriasis, possibly linked with the pathogenesis of this disease.

摘要

为了评估正常和银屑病角质形成细胞中各种碳水化合物的存在和分布,使用几种凝集素(欧洲荆豆,UEA-1;双花扁豆,DBA;单叶豆,BS-I;刀豆球蛋白A,Con A;普通小麦,WGA;蓖麻,RCA;花生,PNA)对11份正常皮肤活检标本和24份银屑病皮损活检标本进行了组织化学检查。研究结果显示,银屑病皮损中的角质形成细胞的特征在于其质膜中所含碳水化合物残基的组成不同。特别是,α-L-岩藻糖、α-D-甘露糖和α-D-葡萄糖向质膜的细胞内转运受到阻碍,而它们在银屑病角质形成细胞质中的合成基本未改变。此外,由于缺乏末端α-L-岩藻糖,α-D-N-乙酰半乳糖胺和α-D-半乳糖残基无法转移到质膜上,因此,银屑病表皮中A和B血型的抗原仍然不完整。基于这些发现,并与我们小组之前关于增殖过度的恶性角质形成细胞的研究结果进行比较,得出的结论是,特别是携带α-L-岩藻糖的糖缀合物的细胞质转运紊乱可能代表银屑病的一种特定缺陷,可能与该疾病的发病机制有关。

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