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患有宿主抗移植物综合征的亲代/ F小鼠嵌合体中的血管内纤维蛋白沉积、肝梗死和血小板减少症。

Intravascular fibrin deposits, hepatic infarcts and thrombocytopenia in parent/F mouse chimeras with host-versus-graft syndrome.

作者信息

Hard R C, Still W J

出版信息

Am J Pathol. 1975 Apr;79(1):131-46.

PMID:1124797
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1912648/
Abstract

Host-versus-graft (HVG) disease is the fatal result of the allogenic reaction which occurs in parental strain mice perinatally inoculated with F(1) hybrid spleen cells. The principal manifestations of the syndrome in RFM/(T(6) X RFM)F(1) mice are thrombocytopenia, intestinal hemorrhage, hepatic necrosis, lymphoproliferative disorders and renal disease due to immune complexes. The discovery of intravascular fibrin deposits in the present studies establishes disseminated intravascular coagulation (DIC) as an intermediary mechanism of HVG disease. It is suggested that the characteristic declines in blood platelet levels, intestinal hemorrhages and hepatic infarcts are triggered principally by immune complexes. Cellular infiltrates of the liver, granulocytosis and hypergammaglobulinemia are other abnormalities which are regularly found in HVG mice and which are also thought to predispose to DIC.

摘要

宿主抗移植物（HVG）病是在围产期接种F(1)杂交脾细胞的亲本品系小鼠中发生的同种异体反应的致命结果。在RFM/(T(6)×RFM)F(1)小鼠中，该综合征的主要表现为血小板减少、肠道出血、肝坏死、淋巴增殖性疾病以及由免疫复合物引起的肾脏疾病。本研究中血管内纤维蛋白沉积的发现确立了弥散性血管内凝血（DIC）作为HVG病的一种中间机制。提示血小板水平的特征性下降、肠道出血和肝梗死主要由免疫复合物触发。肝脏的细胞浸润、粒细胞增多和高球蛋白血症是HVG小鼠中经常发现的其他异常情况，也被认为易引发DIC。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/6cb9f2eb00a5/amjpathol00461-0149-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/62369d381eaf/amjpathol00461-0151-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/d8a6b83bc63f/amjpathol00461-0151-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/39e6f3d86cab/amjpathol00461-0152-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/e81511f0a0c5/amjpathol00461-0152-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/bd150f91b358/amjpathol00461-0149-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/6cb9f2eb00a5/amjpathol00461-0149-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/62369d381eaf/amjpathol00461-0151-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/d8a6b83bc63f/amjpathol00461-0151-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/39e6f3d86cab/amjpathol00461-0152-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/e81511f0a0c5/amjpathol00461-0152-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/bd150f91b358/amjpathol00461-0149-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2487/1912648/6cb9f2eb00a5/amjpathol00461-0149-b.jpg

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引用本文的文献

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3
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Unfractionated spleen cells but not natural killer (NK) cells from RFM donors prevent the progression of host-versus-graft disease in murine RFM/(T6 x RFM)F1 chimeras.来自辐射嵌合体小鼠（RFM）供体的未分级脾细胞而非自然杀伤（NK）细胞，可阻止宿主抗移植物疾病在鼠RFM/（T6×RFM）F1嵌合体中的进展。
Immunology. 1988 Mar;63(3):457-64.
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Hyperimmunoglobulinaemia, T-cell deficiency and plasmacytosis in RFM mice with host versus graft disease induced by the perinatal inoculations (T6XRFM)F1 spleen cells.围产期接种（T6XRFM）F1脾细胞诱导的移植物抗宿主病的RFM小鼠出现高免疫球蛋白血症、T细胞缺陷和浆细胞增多。
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Electron microscopic appearance of fibrin in thin sections.薄切片中纤维蛋白的电子显微镜外观。
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The defibrination syndrome: clinical features and laboratory diagnosis.去纤维蛋白原综合征：临床特征与实验室诊断
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