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实验性自身免疫性神经炎大鼠中核因子-κB 配体⁺细胞的病灶浸润。

Lesional infiltration of receptor activator of nuclear factor-κB ligand⁺ cells in experimental autoimmune neuritis rats.

机构信息

Department of Rehabilitation Medicine, 2nd Affiliated Hospital of Chongqing Medical University, Chongqing 400010, People's Republic of China.

出版信息

Neurol Sci. 2013 Jun;34(6):905-9. doi: 10.1007/s10072-012-1154-2. Epub 2012 Jul 19.

Abstract

Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune demyelinating inflammatory disease of the peripheral nervous system. Receptor activator of NF-κB ligand (RANKL), a member of the tumor necrosis factor family, regulates proliferation of mature T cells. Here, we have studied the expression of RANKL in sciatic nerves of EAN rats. EAN was induced in male Lewis rats. The spatiotemporal expression of RANKL in sciatic nerves of EAN rats was investigated using immunohistochemistry. In sciatic nerves of normal rats RANKL(+) cells were rarely seen. EAN induced a significant accumulation of RANKL(+) cells in sciatic nerves and there was a significant positive correlation of the time course of RANKL(+) cell accumulations with neurological scores of EAN rats. The major cellular resources of RANKL in sciatic nerves were T cells and macrophages. The positive association of RANKL(+) cell accumulations with neurological scores of EAN rats together with the known functions of RANKL indicated that RANKL might play a role in pathologic development of EAN and need further investigation.

摘要

实验性自身免疫性神经炎(EAN)是一种 T 细胞介导的自身免疫性脱髓鞘炎症性周围神经系统疾病。核因子-κB 受体激活剂配体(RANKL)是肿瘤坏死因子家族的一员,调节成熟 T 细胞的增殖。在这里,我们研究了 EAN 大鼠坐骨神经中 RANKL 的表达。雄性 Lewis 大鼠诱导 EAN。使用免疫组织化学研究 EAN 大鼠坐骨神经中 RANKL 的时空表达。在正常大鼠的坐骨神经中很少见到 RANKL(+)细胞。EAN 诱导坐骨神经中 RANKL(+)细胞的大量积聚,并且 RANKL(+)细胞积聚的时间进程与 EAN 大鼠的神经评分呈显著正相关。坐骨神经中 RANKL 的主要细胞来源是 T 细胞和巨噬细胞。RANKL(+)细胞积聚与 EAN 大鼠神经评分的正相关以及 RANKL 的已知功能表明,RANKL 可能在 EAN 的病理发展中起作用,需要进一步研究。

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