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皮肤照射与系统性移植物抗宿主病协同作用,产生皮肤病变。

Irradiation of the skin and systemic graft-versus-host disease synergize to produce cutaneous lesions.

作者信息

Desbarats J, Seemayer T A, Lapp W S

机构信息

Department of Physiology, McGill University, Montreal, Quebec, Canada.

出版信息

Am J Pathol. 1994 May;144(5):883-8.

PMID:8178940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1887374/
Abstract

In this report, the relationship between irradiation and graft-versus-host disease (GVHD)-induced cutaneous injury was investigated. Unirradiated F1 hybrid mice were grafted with irradiated skin and then injected with parental strain lymphoid cells to induce GVHD. Although low grade dermal lymphoid infiltrates were observed in unirradiated skin grafts of some GVH-reactive mice, and irradiated grafts of normal animals showed occasional fibrosis, only the irradiated grafts of GVH-reactive mice developed lesions consisting of vacuolar degeneration of the epidermal-dermal junction and necrotic keratinocytes accompanied by pronounced epidermal infiltrates, characteristic of clinical cutaneous GVHD. The results suggest that cutaneous irradiation exerts a permissive effect on lesion formation in the skin of mice undergoing GVHD. Furthermore, systemic irradiation, known to exacerbate the severity of GVHD, is not required. Cutaneous lesions may be triggered by radiation injury of keratinocytes, up-regulation of adhesion molecules on irradiated endothelium, destruction of protective radiosensitive intraepithelial lymphocytes, and radiation-induced priming of intradermal macrophages.

摘要

在本报告中,研究了辐照与移植物抗宿主病(GVHD)诱导的皮肤损伤之间的关系。未辐照的F1杂种小鼠移植辐照过的皮肤,然后注射亲代品系淋巴细胞以诱导GVHD。虽然在一些GVH反应性小鼠的未辐照皮肤移植物中观察到低度真皮淋巴细胞浸润,正常动物的辐照移植物偶尔出现纤维化,但只有GVH反应性小鼠的辐照移植物出现了由表皮-真皮交界处空泡变性和坏死角质形成细胞组成的病变,并伴有明显的表皮浸润,这是临床皮肤GVHD的特征。结果表明,皮肤辐照对发生GVHD的小鼠皮肤病变形成具有允许作用。此外,已知会加重GVHD严重程度的全身辐照并非必需。皮肤病变可能由角质形成细胞的辐射损伤、辐照内皮细胞上黏附分子的上调、保护性放射敏感上皮内淋巴细胞的破坏以及辐射诱导的真皮内巨噬细胞致敏引发。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ad/1887374/3813509b28bd/amjpathol00065-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ad/1887374/3813509b28bd/amjpathol00065-0045-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66ad/1887374/3813509b28bd/amjpathol00065-0045-a.jpg

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Increased bactericidal macrophage activity induced by immunological stimuli is dependent on interferon (IFN)-gamma. Interference of anti-IFN-gamma but not anti-IFN-alpha/beta with modulation of macrophage activity caused by lymphocytic choriomeningitis virus infection or systemic graft-vs.-host reactions.免疫刺激诱导的巨噬细胞杀菌活性增强依赖于干扰素(IFN)-γ。抗IFN-γ而非抗IFN-α/β干扰淋巴细胞性脉络丛脑膜炎病毒感染或全身性移植物抗宿主反应引起的巨噬细胞活性调节。
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