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血小板衍生因子增强皮肤器官培养中的天疱疮棘层松解。

Platelet-derived factors enhance pemphigus acantholysis in skin organ cultures.

作者信息

Hunziker T, Nydegger U E, Lerch P G, Vassalli J D

出版信息

Clin Exp Immunol. 1986 May;64(2):442-9.

PMID:3742881
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1542357/
Abstract

Supernatant fluids were prepared from human platelets (2-2.5 X 10(10)/ml) after sonication of stimulation with cross-linked IgG; together with plasma samples from two patients with different types of pemphigus, they enhanced acantholysis in cultured punch biopsy specimens of human skin. In the absence of pemphigus plasma the platelet-derived materials did not induce acantholysis. The acantholysis-enhancing effect persisted after exhaustive dialysis or heating (56 degrees C, 30 min). The platelet-derived materials did not contain plasminogen activator; plasminogen itself was detectable by zymographic analysis, although in quantities too low (0.2-0.5 micrograms/ml) to account for the acantholysis-enhancing activity. We conclude that the platelet could contribute to the pathogenesis of pemphigus. The nature of the platelet-derived acantholysis-enhancing factors is presently unknown.

摘要

用交联IgG刺激人血小板(2 - 2.5×10¹⁰/毫升)后超声处理制备上清液;与两名不同类型天疱疮患者的血浆样本一起,它们增强了人皮肤培养打孔活检标本中的棘层松解。在没有天疱疮血浆的情况下,血小板衍生物质不会诱导棘层松解。经过彻底透析或加热(56℃,30分钟)后,棘层松解增强作用仍然存在。血小板衍生物质不含纤溶酶原激活剂;通过酶谱分析可检测到纤溶酶原本身,尽管其含量过低(0.2 - 0.5微克/毫升),无法解释棘层松解增强活性。我们得出结论,血小板可能在天疱疮的发病机制中起作用。目前尚不清楚血小板衍生的棘层松解增强因子的性质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/784a/1542357/de3647c65063/clinexpimmunol00122-0225-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/784a/1542357/a6aa1767e8a4/clinexpimmunol00122-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/784a/1542357/de3647c65063/clinexpimmunol00122-0225-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/784a/1542357/a6aa1767e8a4/clinexpimmunol00122-0222-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/784a/1542357/de3647c65063/clinexpimmunol00122-0225-a.jpg

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1
Platelet-derived factors enhance pemphigus acantholysis in skin organ cultures.血小板衍生因子增强皮肤器官培养中的天疱疮棘层松解。
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2
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Involvement of urokinase-type plasminogen activator in acantholysis induced by pemphigus IgG.尿激酶型纤溶酶原激活剂在天疱疮IgG诱导的棘层松解中的作用。
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J Lab Clin Med. 1988 Jan;111(1):28-34.

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2
Gene Expression Analysis Reveals Novel Shared Gene Signatures and Candidate Molecular Mechanisms between Pemphigus and Systemic Lupus Erythematosus in CD4 T Cells.基因表达分析揭示了天疱疮和系统性红斑狼疮在CD4 T细胞中的新型共享基因特征及候选分子机制。
Front Immunol. 2018 Jan 17;8:1992. doi: 10.3389/fimmu.2017.01992. eCollection 2017.
3
Experimental human cell and tissue models of pemphigus.

本文引用的文献

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ORGAN CULTURE OF ADULT HUMAN SKIN.成人人类皮肤的器官培养
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Plasmin induces acantholysis in skin organ cultures.纤溶酶可在皮肤器官培养物中诱导棘层松解。
Arch Dermatol Res. 1987;279(5):341-6. doi: 10.1007/BF00431228.
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Pemphigus provoked by D(-)penicillamine. An experimental approach using in vitro tissue cultures.青霉胺诱发的天疱疮。一种使用体外组织培养的实验方法。
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Bactericidal activity and chemotaxis in pemphigus vulgaris and bullous pemphigoid.寻常型天疱疮和大疱性类天疱疮中的杀菌活性和趋化作用。
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Methylprednisolone inhibits pemphigus acantholysis in skin cultures.
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Isolation and purification of a pemphigus vulgaris antigen from human epidermis.从人表皮中分离和纯化寻常型天疱疮抗原。
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8
Anti-cell surface pemphigus autoantibody stimulates plasminogen activator activity of human epidermal cells. A mechanism for the loss of epidermal cohesion and blister formation.抗细胞表面天疱疮自身抗体刺激人表皮细胞的纤溶酶原激活物活性。一种表皮黏附丧失和水疱形成的机制。
J Exp Med. 1983 Jan 1;157(1):259-72. doi: 10.1084/jem.157.1.259.
9
Acantholysis produced in vitro with pemphigus serum: hydrocortisone inhibits acantholysis, while dapsone and 6-mercaptopurine do not inhibit acantholysis.天疱疮血清在体外产生的棘层松解:氢化可的松抑制棘层松解,而氨苯砜和6-巯基嘌呤不抑制棘层松解。
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10
Penicillamine-induced pemphigus. Immunoglobulin from this patient induces plasminogen activator synthesis by human epidermal cells in culture: mechanism for acantholysis in pemphigus.青霉胺诱发的天疱疮。该患者的免疫球蛋白可诱导培养的人表皮细胞合成纤溶酶原激活物:天疱疮棘层松解的机制。
Arch Dermatol. 1984 Jun;120(6):762-4. doi: 10.1001/archderm.120.6.762.