摘要
目的探讨新型Th22细胞在多发性硬化(MS)免疫发病机制中的作用。方法 Lewis大鼠后足跖皮下注射髓鞘碱性蛋白(MBP)制备实验性自身免疫性脑脊髓炎(EAE)动物模型,应用BD FACSAria高速流式细胞分选仪无菌分选其脾脏Th22细胞,分析EAE病程不同阶段脾脏Th22细胞分化情况;应用ELISA试剂盒检测EAE病程不同阶段外周血单个核细胞和脾脏单个核细胞中IL-22的分泌水平。结果 EAE发病高峰期Th22细胞的比率(15.23±4.74%)显著高于对照组(1.87±0.89%)、无症状诱导期(7.51±2.66%)、缓解期(8.47±3.39%)和缓解后期(3.56±2.30%),差异均有显著性(P<0.05),表明大鼠致敏后Th22细胞分化逐渐增加,至病程高峰期分化亦达高峰,进入缓解期后则逐渐下降。大鼠外周血单个核细胞及脾脏单个核细胞中IL-22的分泌水平在EAE病程不同阶段呈规律性变化,发病高峰期IL-22分泌水平显著高于其他各期(P<0.05),而对照组及缓解后期则几乎检测不到IL-22分泌。结论Th22细胞及其效应因子IL-22介导EAE发病,揭示了MS发病机制及治疗的新靶点。
Objective To explore the role of Th22 cells in the immunopathogenesis of multiple sclerosis.Methods The experimental autoimmune encephalomyelitis(EAE) models were made by immunizing of Lewis rats with myelin basic protein(MBP).The splenic Th22 cells were separated by BD FACSAria high-speed cell sorter.The differentiation of splenic Th22 cells during the different stages of EAE were analyzed by BD FACSAria.The levels of IL-22 were detected by ELISA Kit in peripheral blood mononuclear cells and splenic mononuclear cells during the different stages of EAE.Results The frequency of Th22 cells at the peak of EAE(15.23 ± 4.74%) was higher than those in normal controls(1.87 ± 0.89%),symptom-free induced phase(7.51 ±2.66%),recovery phase(8.47 ±3.39%) and post-recovery phase(3.56 ±2.30%)(P < 0.05).The differentiation of splenic Th22 cells increased in immunized rats,highest at the peak of EAE,whereas decreased during the recovery phase of EAE.The expression of IL-22 was highest at the peak of EAE both in peripheral blood mononuclear cells and splenic mononuclear cells(P < 0.05).IL-22 was not detected in normal controls and post-recovery phase of EAE.Conclusion Th22 cells and their effector cytokines(IL-22) may participate in the pathogenesis of multiple sclerosis.
出处
《临床和实验医学杂志》
2018年第3期234-238,共5页
Journal of Clinical and Experimental Medicine
基金
首都医科大学基础-临床科研合作基金资助项目(编号:13JL31)
