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移植物抗宿主反应和移植物抗宿主病。

Graft-versus-host reaction and GvH disease.

作者信息

Harada T

机构信息

Department of Pathology I, Shimane Medical University, Izumo, Japan.

出版信息

Tohoku J Exp Med. 1994 May;173(1):171-81. doi: 10.1620/tjem.173.171.

Abstract

Chronic GvHR was induced by inoculating parental lymphoid cells into F1 hybrid mouse. Combination of ATL and ATH, which were congenic recombinant strains differing only in H-2I and S region from each other, was chosen to induce class II-GvHR. Selective activation against partner's alloantigen of graft CD4+ T cells was the primary event of the GvHR and then led to concomitant activation of both graft and host cells. Immune dysregulation among these cells made the GvHR-mouse express various chronic diseases including immune complex glomerulonephritis, autoimmune-like lesions of the liver or the salivary gland, tumor-like proliferations of T cells and abnormal extramedullary hematopoiesis. Chronic GvHR was also induced by a preferential but not a selective activation of graft CD4+ T cells. A combination of DBA/2 and C57BL/6, which differ in whole MHC antigens, was an example. When D2 cells, but not B6 cells, were incoulated into the BDF1 mouse, predominant activation of CD4+ cells over CD8+ cells were observed. Contributing factors to this phenomenon were low responsiveness of graft CD8+ T cells to allogeneic class I MHC antigens and anti-parent activity of host CD8+ cells. Thus both graft and host cells participate either actively or passively in the reaction induced in the parent --> F1 experimental system of GvHR/D.

摘要

通过将亲代淋巴细胞接种到F1杂种小鼠中诱导慢性移植物抗宿主反应(GvHR)。选择仅在H-2I和S区域彼此不同的同基因重组菌株ATL和ATH的组合来诱导II类GvHR。移植物CD4 + T细胞针对伙伴同种异体抗原的选择性激活是GvHR的主要事件,然后导致移植物和宿主细胞的同时激活。这些细胞之间的免疫失调使GvHR小鼠表现出各种慢性疾病,包括免疫复合物肾小球肾炎、肝脏或唾液腺的自身免疫样病变、T细胞的肿瘤样增殖以及异常的髓外造血。慢性GvHR也可由移植物CD4 + T细胞的优先而非选择性激活诱导。例如,全MHC抗原不同的DBA/2和C57BL/6的组合。当将D2细胞而非B6细胞接种到BDF1小鼠中时,观察到CD4 +细胞相对于CD8 +细胞的主要激活。导致这种现象的因素是移植物CD8 + T细胞对同种异体I类MHC抗原的低反应性以及宿主CD8 +细胞的抗亲代活性。因此,在亲代→F1的GvHR/D实验系统中诱导的反应中,移植物和宿主细胞均主动或被动地参与。

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