Human allogeneic vascular rejection after arterial transplantation and peripheral lymphoid reconstitution in severe combined immunodeficient mice.
Human allogeneic vascular rejection after arterial transplantation and peripheral lymphoid reconstitution in severe combined immunodeficient mice.
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严重联合免疫缺陷小鼠动脉移植和外周淋巴重建后的人同种异体血管排斥反应。
DOI：
10.1097/00007890-199903270-00018
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发表时间：
1999
期刊：
影响因子：
6.2
通讯作者：
Pober,JS
中科院分区：
文献类型：
--
作者：
Lorber,MI;Wilson,JH;Robert,ME;Schechner,JS;Kirkiles,N;Qian,HY;Askenase,PW;Tellides,G;Pober,JS
背景：种间差异造成了现有的用于描述体内同种异体移植排斥反应的动物模型的重要缺陷。在接受同种异体人外周血单核细胞（PBMC）的人皮肤移植严重联合免疫缺陷（SCID）小鼠中，已证实了人真皮微血管的同种免疫破坏，组织学上与排斥反应一致。我们现在已经在血管化的，SCID-人动脉移植模型中记录了人类同种免疫损伤。17 SCID/米色小鼠肾下主动脉。结果：49只小鼠中有46只（94%）存活，其中14只为对照组，动脉移植物未接受PBMC。在PBMC给药后14天，32只小鼠中有28只显示循环人CD 3+细胞。在接受同种异体PBMC后14、21或28天处死动物，并回收动脉用于组织学和免疫组织学。所有14只对照小鼠的移植物均通畅，血管组织学正常，无淋巴浸润。在一些动物中，淋巴细胞移植小鼠中移植动脉的损伤在第14天和第21天是明显的，而22只中有16只在第28天表现出中度至重度内膜、中膜和/或外膜淋巴细胞浸润伴内膜扩张。浸润物由HLA-A、-B、-C+和-DR+、人CD 3+细胞组成，大致均匀分布为CD 4+和CD 8+亚群。穿孔素染色显示部分浸润淋巴细胞为溶细胞性细胞。移植的人动脉内皮细胞呈内皮样增生，抗HLA-A、-B、-C和抗HLA-DR抗体染色较强。扩张的内膜主要是平滑肌细胞，平滑肌α-肌动蛋白，HLA-A，-B，-C和HLA-DR染色阳性。未观察到中膜坏死。
Background.Interspecies differences create important shortcomings in existing animal models used to describe in vivo events responsible for allograft rejection. Alloimmune destruction of human dermal microvessels, histologically consistent with rejection, has been demonstrated in human skin-grafted severe combined immunodeficient (SCID) mice receiving allogeneic human peripheral blood mononuclear cells (PBMC). We have now documented human alloimmune injury in a vascularized, SCID-human arterial transplantation model.Methods.Fresh human artery was used to replace the CB. 17 SCID/beige mouse infrarenal aorta. Seven days later, 3× 10 8 human PBMC were administered intraperitoneally, and lymphocyte engraftment was considered successful when circulating human CD3+ cells were later identified in peripheral blood.Results.Forty-six of 49 (94%) mice undergoing transplantation survived, including 14 controls with arterial grafts receiving no PBMC. Twenty-eight of 32 mice demonstrated circulating human CD3+ cells, 14 days after PBMC administration. Animals were killed at 14, 21, or 28 days after receiving allogeneic PBMC, and arteries were recovered for histology and immunohistology. All 14 control mice had patent transplanted grafts with normal vascular histology and no lymphoid infiltration. Damage to transplanted arteries among lymphocyte-engrafted mice was apparent by 14 and 21 days in some animals, whereas 16 of 22 exhibited moderate to severe intimal, medial, and/or adventitial lymphocytic infiltration with intimal expansion by day 28. The infiltrate consisted of HLA-A,-B,-C+, and-DR+, human CD3+ cells, approximately equally distributed as CD4+ and CD8+ subsets. Some infiltrating lymphocytes were cytolytic cells as demonstrated by perforin staining. The endothelium of transplanted human arteries exhibited endothelialitis, and the endothelial cells stained intensely with anti-HLA-A,-B,-C and anti-HLA-DR antibodies. The expanded intima was predominantly smooth muscle cells, staining positively for smooth muscle α-actin, HLA-A,-B,-C and HLA-DR. Medial necrosis was not observed.Conclusion.The results provide evidence of alloimmune-mediated vascular rejection in this human arterial transplantation model.
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影响因子：
19.6
作者：
SOLEZ, K;AXELSEN, RA;YAMAGUCHI, Y
通讯作者：
YAMAGUCHI, Y
人外周血淋巴细胞重建严重联合免疫缺陷 (hu-PBL-SCID) 小鼠：人胰岛同种异体移植排斥模型
影响因子：
6.2
作者：
R. Shiroki;N. Poindexter;E. Woodle;M. Hussain;T. Mohanakumar;D. Scharp
通讯作者：
D. Scharp
慢性同种异体肾移植排斥的可逆性：移植后时间的关键影响表明进行性损伤的宿主免疫依赖性和独立阶段1
影响因子：
6.2
作者：
S. Tullius;W. Hancock;U. Heemann;H. Azuma;N. Tilney
通讯作者：
N. Tilney
心脏移植受者的动脉硬化加速与 T 淋巴细胞介导的内皮炎有关。
影响因子：
6
作者：
R. Hruban;W. Beschorner;William A. Baumgartner;Sharon M. Augustine;Hua Ren;Bruce A. Reitz;G. Hutchins
通讯作者：
G. Hutchins
人肾同种异体移植物中的细胞毒性和细胞凋亡：具有细胞毒性颗粒蛋白 GMP-17 (TIA-1) 的细胞和具有碎片核 DNA 的细胞的鉴定、分布和定量。
DOI：
--
发表时间：
1997
期刊：
Laboratory investigation; a journal of technical methods and pathology
影响因子：
--
作者：
Meehan,SM;McCluskey,RT;Pascual,M;Preffer,FI;Anderson,P;Schlossman,SF;Colvin,RB
通讯作者：
Colvin,RB