Interleukin-1β promotes repair of the CNS
Interleukin-1β promotes repair of the CNS
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DOI：
10.1523/jneurosci.21-18-07046.2001
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发表时间：
2001-09-15
影响因子：
5.3
通讯作者：
Matsushima, GK
中科院分区：
文献类型：
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作者：
Mason, JL;Suzuki, K;Matsushima, GK
白介素1β(IL-1β)是一种促炎细胞因子，与多发性硬化症和中枢神经系统病毒感染等脱髓鞘疾病的病理生理相关。然而，我们在这里证明，IL-1β似乎促进了成人中枢神经系统的重新髓鞘形成。在IL-1β(-/-)小鼠中，急性脱髓鞘进展与野生型小鼠相似，表现为成熟的少突胶质细胞耗竭、小胶质细胞-巨噬细胞聚集和出现少突胶质细胞前体。相比之下，IL-1β(-/-)小鼠未能正确地重新髓鞘，这似乎与小胶质细胞-巨噬细胞和星形胶质细胞缺乏胰岛素样生长因子-1(IGF-1)，以及前体分化为成熟的少突胶质细胞的严重延迟有关。因此，IL-1β可能对中枢神经系统的修复至关重要，可能是通过诱导星形胶质细胞和小胶质细胞-巨噬细胞衍生的IGF-1。
Interleukin-1 beta (IL-1 beta) is a proinflammatory cytokine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and viral infections of the CNS. However, we demonstrate here that IL-1 beta appears to promote remyelination in the adult CNS. In IL-1 beta (-/-) mice, acute demyelination progressed similarly to wild-type mice and showed parallel mature oligodendrocyte depletion, microglia-macrophage accumulation, and the appearance of oligodendrocyte precursors. In contrast, IL-1 beta (-/-) mice failed to remyelinate properly, and this appeared to correlate with a lack of insulin-like growth factor-1 (IGF-1) production by microglia-macrophages and astrocytes and to a profound delay of precursors to differentiate into mature oligodendrocytes. Thus, IL-1 beta may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia-macrophage-derived IGF-1.