中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (8): 1338-1342.doi: 10.4103/1673-5374.162771

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

神经轴突再生障碍:配对免疫球蛋白样受体B

  

  • 收稿日期:2015-04-15 出版日期:2015-08-24 发布日期:2015-08-24
  • 基金资助:

    国家自然科学基金(81170577)

Axon regeneration impediment: the role of paired immunoglobulin-like receptor B

Jing Liu1, Yan Wang1, 2, Wei Fu1, 2   

  1. 1 Neonatal Intensive Care Center, BAYI Children’s Hospital, Beijing Military General Hospital of Chinese PLA, Beijing, China
    2 Graduate School, Southern Medical University, Guangzhou, Guangdong Province, China
  • Received:2015-04-15 Online:2015-08-24 Published:2015-08-24
  • Contact: Jing Liu, M.D., liujingbj@live.cn.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81170577.

摘要:

中枢神经系统损伤后的再生能力很弱,其主要原因是神经元与轴突在修复过程中促进性微环境的缺如和抑制性微环境的存在。配对免疫球蛋白样受体B是近年来新发现的继神经生长抑制因子受体NgR之后3种髓鞘抑制分子神经生长抑制因子包括 Nogo、髓鞘相关糖蛋白和少突胶质细胞髓鞘糖蛋白的另一种共同受体。同时封闭神经生长抑制因子受体和配对免疫球蛋白样受体B,几乎可以完全消除髓鞘相关抑制分子对轴突再生的阻碍作用。配对免疫球蛋白样受体B参与了神经系统尤其是轴突再生受抑制的重要病理过程,虽然目前研究表明,配对免疫球蛋白样受体B是类似与NgR的一种神经轴突再生抑制因子的受体,但其作用并不与之完全相同,文章对配对免疫球蛋白样受体B的结构、分布、与神经系统常见疾病的关系以及目前已知的机制做了简单综述,总结了配对免疫球蛋白样受体B也分布在神经系统之外的组织细胞中,如免疫系统、造血系统的各级细胞中,免疫调节与血细胞迁移是否参与了抑制轴突再生的过程仍需要进一步的研究。

关键词: 神经再生, 脑损伤, 配对免疫球蛋白样受体B, 神经生长抑制因子受体, 髓鞘抑制分子, 神经轴突, 再生, 神经生长抑制因子, 神经生长抑制因子受体, 髓鞘抑制分子, Rho-ROCK信号转导通路, 国家自然科学基金

Abstract:

Regenerative capacity is weak after central nervous system injury because of the absence of an enhancing microenvironment and presence of an inhibitory microenvironment for neuronal and axonal repair. In addition to the Nogo receptor (NgR), the paired immunoglobulin-like receptor B (PirB) is a recently discovered coreceptor of Nogo, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein. Concurrent blocking of NgR and PirB almost completely eliminates the inhibitory effect of myelin-associated inhibitory molecules on axonal regeneration. PirB participates in a key pathological process of the nervous system, specifically axonal regeneration inhibition. PirB is an inhibitory receptor similar to NgR, but their effects are not identical. This study summarizes the structure, distribution, relationship with common nervous system diseases, and known mechanisms of PirB, and concludes that PirB is also distributed in cells of the immune and hematopoietic systems. Further investigations are needed to determine if immunomodulation and blood cell migration involve inhibition of axonal regeneration.

Key words: nerve regeneration, brain injury, paired immunoglobulin-like receptor B, myelin inhibitory molecule, axons, regeneration, Rho-ROCK signaling pathway, NSFC grant, neural regeneration