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诱导实验性脑型疟疾需要血管细胞上表达肿瘤坏死因子受体2 。

Requirement for tumor necrosis factor receptor 2 expression on vascular cells to induce experimental cerebral malaria.

作者信息

Stoelcker Benjamin, Hehlgans Thomas, Weigl Karin, Bluethmann Horst, Grau Georges E, Männel Daniela N

机构信息

Institute of Pathology/Tumor Immunology, University of Regensburg, 93042 Regensburg, Germany.

出版信息

Infect Immun. 2002 Oct;70(10):5857-9. doi: 10.1128/IAI.70.10.5857-5859.2002.

DOI:10.1128/IAI.70.10.5857-5859.2002
PMID:12228317
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC128326/
Abstract

Using tumor necrosis factor receptor type 2 (TNFR2)-deficient mice and generating bone marrow chimeras which express TNFR2 on either hematopoietic or nonhematopoietic cells, we demonstrated the requirement for TNFR2 expression on tissue cells to induce lethal cerebral malaria. Thus, TNFR2 on the brain vasculature mediates tumor necrosis factor-induced neurovascular lesions in experimental cerebral malaria.

摘要

利用2型肿瘤坏死因子受体（TNFR2）缺陷小鼠并构建在造血细胞或非造血细胞上表达TNFR2的骨髓嵌合体，我们证明了组织细胞上TNFR2的表达对于诱导致死性脑型疟疾是必需的。因此，脑微血管系统上的TNFR2在实验性脑型疟疾中介导肿瘤坏死因子诱导的神经血管病变。

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Tumor necrosis factor induces tumor necrosis via tumor necrosis factor receptor type 1-expressing endothelial cells of the tumor vasculature.肿瘤坏死因子通过肿瘤血管中表达1型肿瘤坏死因子受体的内皮细胞诱导肿瘤坏死。
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The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kDa tumor necrosis factor receptor.肿瘤坏死因子的跨膜形式是80 kDa肿瘤坏死因子受体的主要激活配体。
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