CD8型
细胞毒性T细胞
CXCL10型
细胞生物学
CXCR3型
p38丝裂原活化蛋白激酶
雪旺细胞
生物
免疫印迹
分子生物学
化学
癌症研究
趋化因子
激酶
免疫学
蛋白激酶A
炎症
抗原
趋化因子受体
生物化学
体外
基因
作者
Wei Tang,Qian Lv,Xiangfang Chen,Junjie Zou,Zhimin Liu,Yongquan Shi
摘要
Background: Damage to Schwann cells has been reported in the development of diabetic peripheral neuropathy (DPN), but how Schwann cells are damaged has not been elucidated. Methods: The highly expressed proteins in the PBMC of DPN patients were identified through MALDI-TOF/TOF and SELDI protein chip technology. The expression levels of CXCR3 were detected by qPCR and flow cytometric analysis. Transwell migration assay was to investigate the migration of CD8+ T cells. Western-blot analysis was to detect the levels of p38 MAP kinases pathway related proteins and TNF-α, FasL, and PDL1. Results: Two highly expressed proteins, CXCR3 and p38, were identified. Under high glucose conditions, CXCR3 was elevated in CD8+ T cells via the activation of p38 MAP kinases. Moreover, CXCL9, CXCL10, and CXCL11 expression were induced in Schwann cells, leading to the recruitment and infiltration of CD8+ T cells into DPN tissues. Further study demonstrated that Schwann cells promoted activation of CD8+ T cells and induced expression of TNF-α, FasL, and PDL1 on CD8+ T cells, in return, CD8+ T cells induced obvious apoptosis of Schwann cells. Conclusion: Our study indicates that CD8+ T cells mediate cytotoxicity toward Schwann cells and play an important role in the development of DPN.
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