Burwinkel Michael, Riemer Constanze, Schwarz Anja, Schultz Julia, Neidhold Sabine, Bamme Theresa, Baier Michael
Robert-Koch-Institute, Nordufer 20, 13353 Berlin, Germany.
Int J Dev Neurosci. 2004 Nov;22(7):497-505. doi: 10.1016/j.ijdevneu.2004.07.017.
Prion infections of the central nervous system (CNS) are characterised by a reactive gliosis and the subsequent degeneration of neuronal tissue. The activation of glial cells, which precedes neuronal death, is likely to be initially caused by the deposition of misfolded, proteinase K-resistant, isoforms (termed PrP(res)) of the prion protein (PrP) in the brain. Cytokines and chemokines released by PrP(res)-activated glia cells may contribute directly or indirectly to the disease development by enhancement and generalisation of the gliosis and via cytotoxicity for neurons. However, the actual role of prion-induced glia activation and subsequent cytokine/chemokine secretion in disease development is still far from clear. In the present work, we review our present knowledge concerning the functional biology of cytokines and chemokines in prion infections of the CNS.
中枢神经系统（CNS）的朊病毒感染的特征是反应性胶质增生以及随后的神经元组织退化。在神经元死亡之前发生的胶质细胞激活，最初可能是由错误折叠的、蛋白酶K抗性的朊病毒蛋白（PrP）异构体（称为PrP（res））在大脑中的沉积引起的。PrP（res）激活的胶质细胞释放的细胞因子和趋化因子可能通过增强和泛化胶质增生以及对神经元的细胞毒性直接或间接促进疾病发展。然而，朊病毒诱导的胶质细胞激活以及随后细胞因子/趋化因子分泌在疾病发展中的实际作用仍远未明确。在本研究中，我们综述了目前关于细胞因子和趋化因子在中枢神经系统朊病毒感染中的功能生物学的知识。
