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The lpr and gld genes in systemic autoimmunity: life and death in the Fas lane.

作者信息

Cohen P L, Eisenberg R A

机构信息

Dept of Medicine, University of North Carolina School of Medicine, Chapel Hill 27599-7280.

出版信息

Immunol Today. 1992 Nov;13(11):427-8. doi: 10.1016/0167-5699(92)90066-G.

DOI:10.1016/0167-5699(92)90066-G
PMID:1282318
Abstract

The single gene lpr and gld models of spontaneous systemic autoimmunity have attracted much attention in recent years. Here, Philip Cohen and Robert Eisenberg describe the fascinating recent findings that the lpr and gld [corrected] phenotypes result from defects in the Fas gene and, perhaps, in the ligand for fas, respectively.

摘要

相似文献

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The lpr and gld genes in systemic autoimmunity: life and death in the Fas lane.
Immunol Today. 1992 Nov;13(11):427-8. doi: 10.1016/0167-5699(92)90066-G.
2
Apoptosis abnormalities of splenic lymphocytes in autoimmune lpr and gld mice.自身免疫性lpr和gld小鼠脾脏淋巴细胞的凋亡异常
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gld/gld mice are unable to express a functional ligand for Fas.gld/gld小鼠无法表达功能性Fas配体。
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Cellular interactions in the lpr and gld models of systemic autoimmunity.系统性自身免疫的lpr和gld模型中的细胞相互作用。
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Murine models of autoimmunity: T-cell and B-cell defects.自身免疫的小鼠模型:T 细胞和 B 细胞缺陷
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Oncogene expression in autoimmune mice.自身免疫小鼠中的癌基因表达。
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In vivo depletion of Thy-1-positive cells originating from normal bone marrow abrogates the suppression of gld disease in normal-gld mixed bone marrow chimeras.体内去除源自正常骨髓的Thy-1阳性细胞可消除正常-gld混合骨髓嵌合体中gld疾病的抑制作用。
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Human autoimmune lymphoproliferative syndrome, a defect in the apoptosis-inducing Fas receptor: a lesson from the mouse model.人类自身免疫性淋巴细胞增生综合征,一种凋亡诱导性Fas受体缺陷:来自小鼠模型的教训。
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Co-infusion of normal bone marrow partially corrects the gld T-cell defect. Evidence for an intrinsic and extrinsic role for Fas ligand.正常骨髓的共同输注可部分纠正gld T细胞缺陷。Fas配体的内在和外在作用的证据。
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