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银屑病斑块“病损周围皮肤”的早期炎症变化:树突状细胞与角质形成细胞之间存在相互作用吗?

Early inflammatory changes in the "perilesional skin" of psoriatic plaques: is there interaction between dendritic cells and keratinocytes?

作者信息

Komine Mayumi, Karakawa Masaru, Takekoshi Tomonori, Sakurai Naoki, Minatani Yosaku, Mitsui Hiroshi, Tada Yayoi, Saeki Hidehisa, Asahina Akihiko, Tamaki Kunihiko

机构信息

Department of Dermatology, University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.

出版信息

J Invest Dermatol. 2007 Aug;127(8):1915-22. doi: 10.1038/sj.jid.5700799. Epub 2007 Apr 19.

DOI:10.1038/sj.jid.5700799
PMID:17446902
Abstract

Early inflammatory changes in psoriatic plaques were investigated immunohistochemically by studying the normal-appearing skin adjacent to the plaques (perilesional skin), lesional skin, and distant uninvolved skin from psoriasis patients. Perilesional epidermis contained numerous CD1a-positive Langerhans cells, some of which expressed HLA-DR, CD83, CD80, and CD86, at the same time expressing Langerin. There were also numerous CD83-positive, CD11c-positive, Langerin-negative dendritic cells (DCs) in the epidermal-dermal junction of perilesional skin. CD3-positive T lymphocytes were sparse in the perilesional skin. Perilesional epidermis expressed keratin K6 and K16, inflammatory keratins, and C/EBPbeta, a transcription factor related to inflammatory cytokines. Our results demonstrated the abundant distribution of activated DCs in the perilesional skin of psoriatic plaques, where early inflammatory changes occur in the epidermal keratinocytes, which suggests their involvement in the provocation of epidermal inflammation in the perilesional epidermis and further pathogenic roles in the formation of psoriatic plaques.

摘要

通过研究银屑病患者斑块周围外观正常的皮肤(病损周围皮肤)、病损皮肤以及远处未受累皮肤,采用免疫组织化学方法对银屑病斑块的早期炎症变化进行了研究。病损周围表皮含有大量CD1a阳性的朗格汉斯细胞,其中一些同时表达HLA-DR、CD83、CD80和CD86,并表达朗格素。在病损周围皮肤的表皮-真皮交界处也有大量CD83阳性、CD11c阳性、朗格素阴性的树突状细胞(DCs)。CD3阳性T淋巴细胞在病损周围皮肤中稀少。病损周围表皮表达角蛋白K6和K16、炎性角蛋白以及C/EBPβ,一种与炎性细胞因子相关的转录因子。我们的结果表明,在银屑病斑块的病损周围皮肤中存在大量活化的DCs,此处表皮角质形成细胞发生早期炎症变化,这提示它们参与了病损周围表皮炎症的激发以及在银屑病斑块形成中进一步的致病作用。

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