Interleukin-1beta promotes repair of the CNS.
Interleukin-1beta promotes repair of the CNS.
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发表时间：
2001
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通讯作者：
J. Mason;K. Suzuki;D. Chaplin;G. Matsushima
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作者：
J. Mason;K. Suzuki;D. Chaplin;G. Matsushima
白细胞介素-1 β (il -1 β)是一种促炎细胞因子，与脱髓鞘疾病（如多发性硬化症和中枢神经系统病毒感染）的病理生理相关。然而，我们在这里证明il -1 β似乎促进成人中枢神经系统的髓鞘再生。在il -1 β(-/-)小鼠中，急性脱髓鞘的进展与野生型小鼠相似，并表现出平行的成熟少突胶质细胞耗竭、小胶质-巨噬细胞积累和少突胶质细胞前体的出现。相反，il -1 β(-/-)小鼠不能正常地再髓鞘化，这似乎与小胶质巨噬细胞和星形胶质细胞缺乏胰岛素样生长因子-1 （IGF-1）的产生以及前体向成熟少突胶质细胞分化的严重延迟有关。因此，il -1 β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-巨噬细胞衍生的IGF-1。
Interleukin-1beta (IL-1beta) 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-1beta appears to promote remyelination in the adult CNS. In IL-1beta(-/-) 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-1beta(-/-) 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-1beta may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia-macrophage-derived IGF-1.