肿瘤坏死因子受体在实验性脑型疟疾发展中的各自作用。
Respective role of TNF receptors in the development of experimental cerebral malaria.
作者信息
Lucas R, Lou J N, Juillard P, Moore M, Bluethmann H, Grau G E
机构信息
Dept. of Anaesthesiology, Pharmacology and Surgical Intensive Care, University Medical Center, Geneva, Switzerland.
出版信息
J Neuroimmunol. 1997 Feb;72(2):143-8. doi: 10.1016/s0165-5728(96)00185-3.
The respective role of the two receptors of TNF in experimental cerebral malaria (CM) was investigated. During CM, a significant upregulation of TNF-receptor 2 (TNFR2), but not of TNFR1, was found in brain microvessels of susceptible, but not resistant mice. Mice genetically deficient for TNFR2 (Tnfr2null) were significantly protected from CM, while TNFR1-deficient (Tfnr1null) mice were as susceptible as wild-type mice. The protection of Tnfr2null mice could be explained by their absence of ICAM-1 upregulation and leukocyte sequestration, known to occur in brain microvessels of CM-susceptible animals.
研究了肿瘤坏死因子（TNF）的两种受体在实验性脑型疟疾（CM）中的各自作用。在CM期间，在易感但非抗性小鼠的脑微血管中发现TNF受体2（TNFR2）显著上调，而TNFR1未上调。基因缺失TNFR2（Tnfr2null）的小鼠对CM有显著保护作用，而缺乏TNFR1（Tfnr1null）的小鼠与野生型小鼠一样易感。Tnfr2null小鼠的保护作用可以通过其脑微血管中不存在已知在CM易感动物中发生的细胞间黏附分子-1（ICAM-1）上调和白细胞滞留来解释。
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