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连续来源的内皮细胞以及体内和体外的树突状细胞/巨噬细胞对MS-1高分子量蛋白的可诱导表达。

Inducible expression of MS-1 high-molecular-weight protein by endothelial cells of continuous origin and by dendritic cells/macrophages in vivo and in vitro.

作者信息

Goerdt S, Bhardwaj R, Sorg C

机构信息

Klinik und Poliklinik für Hautkrankheiten, Westfälische Wilhelms-Universität, Münster/Westfalen, Germany.

出版信息

Am J Pathol. 1993 May;142(5):1409-22.

PMID:8494045
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1886924/
Abstract

Recently, we have described a monoclonal antibody, named MS-1, which identifies a novel high-molecular-weight protein expressed by noncontinuous, sinusoidal endothelia and by interstitial dendritic cells in certain normal human organs (S Goerdt, LJ Walsh, GF Murphy, JS Pober, J Cell Biol 1991, 113:1425-1437; and LJ Walsh, S Goerdt, JS Pober, H Sueki, GF Murphy, Lab Invest 1991, 65: 732-741). In this report, we demonstrate in studying a variety of skin lesions that MS-1 antigen can also be expressed by endothelia of continuous origin under certain pathological conditions. Among the skin lesions tested, MS-1 antigen expression by endothelial cells of continuous origin is frequently observed in wound healing tissue, in cutaneous T-cell lymphoma, in psoriasis, and in melanoma metastasis, ie, in 100%, 80%, 71%, and 71% of cases, respectively. In contrast, endothelial MS-1 antigen expression rarely occurred in other skin lesions, including vascular tumors, six of which were Kaposi's sarcomas (13% and 0% of cases with vascular MS-1 expression, respectively). The percentage of cases with MS-1+ vessels is only marginally different in malignant versus benign lesions (55% versus 31%); when melanocytic nevi, primary melanomas, and melanoma metastases are compared, however, an increase in the percentage of cases with MS-1+ vessels is seen (31%, 50%, and 71%, respectively). Apart from wound healing, the relative number of MS-1+ vessels in a given lesion amounts to less than 5% compared with the number of continuous type vessels stained by monoclonal antibody 1F10 (S Goerdt, F Steckel, K Schulze-Osthoff, H-H Hagemeier, E Macher, C Sorg, Exp Cell Biol 1989, 57: 185-192). In addition, the occurrence of MS-1+ vessels is not related to the overall vascularity of a given lesion. Thus, the conditions for MS-1 antigen expression by endothelia of continuous origin cannot as yet be exactly defined. Furthermore, we have noticed that the number of MS-1+ dendritic cells varies considerably in skin lesions; in the early patch lesions of Kaposi's sarcoma and in juvenile xanthogranuloma MS-1+ cells even constitute the major cell type. This prompted us to investigate MS-1 antigen expression and its regulation in cultured human monocytes/macrophages. Expression of MS-1 antigen by these cells regularly starts at day 3 of culture and reaches its maximal value at day 9, after which it declines.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

最近,我们描述了一种名为MS-1的单克隆抗体,它可识别一种由非连续性窦状内皮细胞以及某些正常人体器官中的间质树突状细胞表达的新型高分子量蛋白(S·戈尔特、L·J·沃尔什、G·F·墨菲、J·S·波伯,《细胞生物学杂志》1991年,第113卷:第1425 - 1437页;以及L·J·沃尔什、S·戈尔特、J·S·波伯、H·末木、G·F·墨菲,《实验医学杂志》1991年,第65卷:第732 - 741页)。在本报告中,我们在研究多种皮肤病变时证明,在某些病理条件下,连续来源的内皮细胞也可表达MS-1抗原。在所测试的皮肤病变中,连续来源的内皮细胞表达MS-1抗原在伤口愈合组织、皮肤T细胞淋巴瘤、银屑病和黑色素瘤转移中经常可见,即在病例中分别占100%、80%、71%和71%。相比之下,内皮细胞MS-1抗原表达在其他皮肤病变中很少发生,包括血管肿瘤,其中6例为卡波西肉瘤(血管MS-1表达病例分别占13%和0%)。MS-1阳性血管的病例百分比在恶性与良性病变中仅有微小差异(55%对31%);然而,当比较黑素细胞痣、原发性黑色素瘤和黑色素瘤转移时,MS-1阳性血管的病例百分比有所增加(分别为31%、50%和71%)。除伤口愈合外,与单克隆抗体1F10染色的连续型血管数量相比,给定病变中MS-1阳性血管的相对数量不到5%(S·戈尔特、F·施泰克尔、K·舒尔茨 - 奥斯特霍夫、H - H·哈格迈尔、E·马赫、C·索尔格,《实验细胞生物学》1989年,第57卷:第185 - 192页)。此外,MS-1阳性血管的出现与给定病变的总体血管分布无关。因此,连续来源的内皮细胞表达MS-1抗原的条件尚未能确切界定。此外,我们注意到MS-1阳性树突状细胞的数量在皮肤病变中差异很大;在卡波西肉瘤的早期斑片病变和幼年黄色肉芽肿中,MS-1阳性细胞甚至构成主要细胞类型。这促使我们研究MS-1抗原在培养的人单核细胞/巨噬细胞中的表达及其调控。这些细胞中MS-1抗原的表达通常在培养第3天开始,在第9天达到最大值,之后下降。(摘要截选至400字)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/ad07ab11207b/amjpathol00077-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/dc18fe99632f/amjpathol00077-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/f415acc873dc/amjpathol00077-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/ad07ab11207b/amjpathol00077-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/dc18fe99632f/amjpathol00077-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/f415acc873dc/amjpathol00077-0089-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/582f/1886924/ad07ab11207b/amjpathol00077-0093-a.jpg

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