[细胞免疫和血管生成变化在局限性硬皮病发病机制中的作用研究]。

IF 0.5 Q4 DERMATOLOGY Przeglad dermatologiczny Pub Date : 1990-07-01
S Majewski, M Błaszczyk, M Chibowska, D Rosińska-Borkowska, D Kencka, L Rudnicka, M Marczak, B Makieła, A Skiendzielewska, S Jabłońska
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引用次数: 0

摘要

对48例morphea患者进行了研究,包括1)抗核抗体2)淋巴细胞诱导血管生成3)自然杀伤(NK)细胞活性和4)外周血T细胞亚群。44.4%(8/18)的线性硬皮病患者和21%(4/19)的弥散性脑脊液患者存在抗核抗体。41.5% (17/41) morphea患者淋巴细胞诱导血管生成增加,主要发生在血管明显改变的病例中。E型莲座形成试验显示,morphea患者外周血活跃莲座形成细胞(ARFC)和总莲座形成细胞(TRFC)百分比下降,NK细胞活性降低。与系统性硬皮病患者的细胞免疫紊乱相比,在morphea患者中获得的这些结果显示出一些相似性和差异性。
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[Studies of the role of cellular immunity and angiogenetic changes in the pathogenesis of circumscribed scleroderma].

The studies were performed in 48 patients with morphea and included evaluation of 1) antinuclear antibodies 2) lymphocyte induced angiogenesis 3) natural killer (NK) cell activity and 4) T cell subpopulations in peripheral blood. The presence of antinuclear antibodies was found in 44.4% (8/18) patients with scleroderma linearis and in 21% (4/19) patients with morphea disseminata. Lymphocyte induced angiogenesis was increased in 41.5% (17/41) morphea patients, mainly in cases with pronounced vascular changes. The E rosette forming test showed a decreased percentage of active rosette forming cells (ARFC) and total rosette forming cells (TRFC) in peripheral blood and the NK cell activity was lowered in patients with morphea. These results obtained in patients with morphea show some similarities and differences in comparison to cellular immunity disturbances in patients with systemic scleroderma.

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来源期刊
CiteScore
0.80
自引率
14.30%
发文量
9
审稿时长
12 weeks
期刊介绍: Przegląd Dermatologiczny (ang. Dermatological Review) is a bimonthly magazine of the Polish Dermatological Association. It publishes original (clinical and experimental) papers, review papers, care reports, reports from congresses, reviews of books, announcements, letters to the editor and special papers (requested by the editors), concerning selected dermatological and interdisciplinary issues. Papers sent to the editor are reviewed.
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