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首页> 外文期刊>The European Journal of Neuroscience >Interleukin-6 (IL6) and cellular response to facial nerve injury: effects on lymphocyte recruitment, early microglial activation and axonal outgrowth in IL6-deficient mice.
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Interleukin-6 (IL6) and cellular response to facial nerve injury: effects on lymphocyte recruitment, early microglial activation and axonal outgrowth in IL6-deficient mice.

机译：白细胞介素6（IL6）和对面神经损伤的细胞反应：对IL6缺陷小鼠淋巴细胞募集，早期小胶质细胞活化和轴突生长的影响。

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摘要

Nerve injury triggers numerous changes in the injured neurons and surrounding non-neuronal cells. Of particular interest are molecular signals that play a role in the overall orchestration of this multifaceted cellular response. Here we investigated the function of interleukin-6 (IL6), a multifunctional neurotrophin and cytokine rapidly expressed in the injured nervous system, using the facial axotomy model in IL6-deficient mice and wild-type controls. Transgenic deletion of IL6 caused a massive decrease in the recruitment of CD3-positive T-lymphocytes and early microglial activation during the first 4 days after injury in the axotomized facial nucleus. This was accompanied by a more moderate reduction in peripheral regeneration at day 4, lymphocyte recruitment (day 14) and enhanced perikaryal sprouting (day 14). Motoneuron cell death, phagocytosis by microglial cells and recruitment of granulocytes and macrophages into injured peripheral nerve were not affected. In summary, IL6 lead to a variety of effects on the cellular response to neural trauma. However, the particularly strong actions on lymphocytes and microglia suggest that this cytokine plays a central role in the initiation of immune surveillance in the injured central nervous system.
机译：神经损伤触发受损神经元和周围非神经元细胞的许多变化。特别令人感兴趣的是在这种多方面细胞应答的整体编排中起作用的分子信号。在这里，我们使用IL6缺陷小鼠的面部轴切模型和野生型对照，研究了在受损神经系统中快速表达的多功能神经营养蛋白和细胞因子白介素6（IL6）的功能。 IL6的转基因缺失在切开后的面神经核损伤后的前4天导致CD3阳性T淋巴细胞的募集和早期小胶质细胞活化大量减少。这伴随着在第4天外周再生更适度的减少，淋巴细胞募集（第14天）和增强的牙周萌芽（第14天）。运动神经元细胞的死亡，小胶质细胞的吞噬作用以及粒细胞和巨噬细胞募集到受损的周围神经中均未受到影响。总之，IL6导致对神经损伤的细胞反应的多种作用。但是，对淋巴细胞和小胶质细胞特别强的作用表明，这种细胞因子在受伤的中枢神经系统的免疫监视启动中起着核心作用。

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