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盘状红斑狼疮和扁平苔藓中角蛋白和兜甲蛋白的表达

Keratin and involucrin expression in discoid lupus erythematosus and lichen planus.

作者信息

Ichikawa E, Watanabe S, Takahashi H

机构信息

Division of Dermatology, Doai Memorial Hospital, Tokyo, Japan.

出版信息

Arch Dermatol Res. 1997 Aug;289(9):519-26. doi: 10.1007/s004030050233.

Abstract

In the present study, keratin and involucrin expression were studied in cutaneous lesions of discoid lupus erythematosus and lichen planus in order to gain a better understanding of the abnormal differentiation or maturation of the epidermal cells in these dermatoses. Ten specimens each from discoid lupus erythematosus and lichen planus were analyzed by immunohistochemical techniques, using a panel of monoclonal antikeratin antibodies and polyclonal anti-involucrin antibody, and five specimens each were analyzed by one- and two-dimensional gel electrophoresis and immunoblot analysis using three antikeratin antibodies. No significant difference was found between the dermatoses. The expression of differentiation-specific keratins showed a similar pattern to that in normal epidermis, and involucrin was expressed even in the lower part of the stratum spinosum. Keratins 6 and 16, which are characteristic markers of hyperproliferative states, and keratin 17 were detected in nonhyperproliferative and atrophic epidermis with hydropic degeneration and inflammatory infiltrates in the dermis. These results suggest that expression of keratins 6, 16 and 17 in discoid lupus erythematosus and lichen planus may reflect a wound healing response to the damage to the basal cell layer, or may be under the control of cytokines produced by infiltrating inflammatory cells in the dermis.

摘要

在本研究中,对盘状红斑狼疮和扁平苔藓的皮肤损害进行了角蛋白和兜甲蛋白表达的研究,以便更好地了解这些皮肤病中表皮细胞的异常分化或成熟情况。采用一组单克隆抗角蛋白抗体和多克隆抗兜甲蛋白抗体,通过免疫组化技术对来自盘状红斑狼疮和扁平苔藓的各10个标本进行了分析,并用三种抗角蛋白抗体通过一维及二维凝胶电泳和免疫印迹分析对各5个标本进行了分析。在这两种皮肤病之间未发现显著差异。分化特异性角蛋白的表达模式与正常表皮相似,甚至在棘层下部也有兜甲蛋白表达。在非增殖性和萎缩性表皮伴真皮水肿性变性和炎症浸润中检测到了作为增殖亢进状态特征性标志物的角蛋白6和16以及角蛋白17。这些结果表明,盘状红斑狼疮和扁平苔藓中角蛋白6、16和17的表达可能反映了对基底细胞层损伤的伤口愈合反应,或者可能受真皮中浸润性炎症细胞产生的细胞因子的调控。

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