TNF-ALPHA SUPPRESSES CR3-MEDIATED MYELIN REMOVAL BY MACROPHAGES
TNF-ALPHA SUPPRESSES CR3-MEDIATED MYELIN REMOVAL BY MACROPHAGES
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DOI：
10.1016/0165-5728(92)90085-y
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发表时间：
1992-05-01
影响因子：
3.3
通讯作者：
FRIEDE, RL
中科院分区：
文献类型：
--
作者：
BRUCK, W;BRUCK, Y;FRIEDE, RL
单核细胞/巨噬细胞系统的单核细胞在沃勒变性期间的髓鞘摄取中起重要作用。目前的体外研究阐明了两种巨噬细胞分泌的细胞因子TNF-α和白细胞介素-1在这一过程中的作用。用TNF-α治疗大大减少了巨噬细胞通过补体受体3型（CR 3）摄取的髓鞘的量。抗TNF-α抗体逆转了这种作用。巨噬细胞的免疫荧光显示TNF-α引起吞噬细胞CR 3表达减少。进一步的实验揭示了TNF-α与巨噬细胞膜上的受体的相互作用。在这些实验中使用的体外系统中，白细胞介素-1对髓鞘摄取没有影响。
Mononuclear cells of the monocyte/macrophage system play an important role in myelin ingestion during Wallerian degeneration. The present in vitro study clarifies the role in this process of two macrophage-secreted cytokines, TNF-alpha and interleukin-1. Treatment with TNF-alpha massively reduced the amount of myelin ingested by macrophages via their complement receptor type 3 (CR3). Anti-TNF-alpha antibodies reversed the effect. Immunofluorescence of macrophages indicated that TNF-alpha caused a reduced expression of the CR3 by phagocytic cells. Further experiments revealed an interaction of TNF-alpha with its receptor on the macrophage cell membrane. Interleukin-1 had no effect on myelin ingestion in the in vitro system used in these experiments.