Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153, USA.
J Neuroimmunol. 2009 Nov 30;216(1-2):66-75. doi: 10.1016/j.jneuroim.2009.09.009. Epub 2009 Oct 8.
We have previously demonstrated a neuroprotective mechanism of facial motoneuron (FMN) survival after facial nerve axotomy that is dependent on CD4(+) Th2 cell interaction with peripheral antigen-presenting cells, as well as CNS resident microglia. To investigate this mechanism, we chose to study the Th2-associated chemokine, CCL11, and Th1-associated chemokine, CXCL11, in wild-type and presymptomatic mSOD1 mice after facial nerve axotomy. In this report, the results indicate that CCL11 is constitutively expressed in the uninjured facial motor nucleus, but CXCL11 is not expressed at all. Facial nerve axotomy induced a shift in CCL11 expression from FMN to astrocytes, whereas CXCL11 was induced in FMN. Differences in the number of CCL11- and CXCL11-expressing cells were observed between WT and mSOD1 mice after facial nerve axotomy.
我们之前已经证明了面神经轴突切断后面运动神经元(FMN)存活的神经保护机制,该机制依赖于 CD4(+)Th2 细胞与外周抗原呈递细胞以及中枢神经系统驻留的小胶质细胞的相互作用。为了研究这一机制,我们选择研究 Th2 相关趋化因子 CCL11 和 Th1 相关趋化因子 CXCL11 在面神经轴突切断后的野生型和发病前 mSOD1 小鼠中的表达。在本报告中,结果表明 CCL11 在未受伤的面运动核中持续表达,但 CXCL11 根本不表达。面神经轴突切断诱导 CCL11 表达从 FMN 转移到星形胶质细胞,而 CXCL11 在 FMN 中被诱导。面神经轴突切断后,在 WT 和 mSOD1 小鼠之间观察到 CCL11 和 CXCL11 表达细胞的数量存在差异。