| 穆莉莉 汤凤彩 李金宝 梁明 王菁华 李呼伦.S100/RAGE 在实验性自身免疫性重症肌无力中对T细胞的作用及其机制研究[J].,2015,15(30):5825-5829 |
| S100/RAGE 在实验性自身免疫性重症肌无力中对T细胞的作用及其机制研究 |
| Research on the Effects and Mechanisms of S100/RAGE on the T Cell ofExperimental Autoimmune Myasthenia Gravis |
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| DOI： |
| 中文关键词: RAGE S100B 实验性自身免疫性重症肌无力 T细胞 Th 细胞亚型 |
| 英文关键词: RAGE S100B EAMG T cell Th subset |
| 基金项目:黑龙江省教育厅科学技术研究项目（12521213） |
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| 中文摘要: |
| 目的：探讨RAGE 及其配体S100B 在实验性自身免疫性重症肌无力(EAMG)中对T 细胞的作用及其相关机制。方法：选取体
重160-180g 的Lewis 大鼠，并将其随机分为EAMG 模型组和CFA 对照组。EAMG 模型组大鼠通过尾根部注入200 滋L 含有
R-AChR97-116 肽段的免疫乳剂，并于初始免疫后的第30 天尾根部追加免疫一次；CFA 对照组大鼠为免疫乳剂中不含有
R-AChR97-116 肽段。采用流式细胞术检测和比较两组大鼠CD4+T 细胞上RAGE 的表达情况；ELISA 方法检测淋巴细胞培养上
清中IFN-r、IL-4、IL-17、TGF-beta、IL-6 和S100B 的表达水平；采用S100B 体外干预淋巴细胞，进一步检测S100B 对EAMG 大鼠T
细胞增殖、亚型分布、细胞因子分泌的影响。结果：在疾病发生的晚期时相(初次免疫后第45天)，EAMG 组淋巴细胞CD4+T细胞
上RAGE 的表达明显高于CFA 组(P<0.001)，血清中RAGE 的配体S100B的表达也高于CFA 组(P<0.001)；体外加入S100B 干预
能促进T 淋巴细胞的增殖，与未干预组相比较差异显著(P<0.05)；S100B刺激后，Th1 细胞和Th17 细胞的百分比进一步增高，Th2
细胞和Treg 细胞百分比下降(PTh1<0.05，PTh17<0.05，PTh2>0.05，PTreg<0.05)，IFN-r和IL-17 的表达上调(PIFN-r<0.05，PIL-17<0.05)，而IL-4
和TGF-beta表达下降(PTGF-beta<0.01，PIL-4>0.05)，Th17 细胞的调控因子IL-6 表达升高(PIL-6<0.05)。结论：RAGE 及其配体S100B 参与
EAMG 的发病过程，在晚期时相中表现出明显的致病性；RAGE 与S100B 相互作用可以上调T 细胞的致病性作用，加重四种辅助
性T 细胞之间的网络失衡。 |
| 英文摘要: |
| Objective:To establish a rat model of experimental autoimmune myasthenia gravis (EAMG) and study the effects and
mechanisms of S100/RAGE on the T Cell of EAMG.Methods:Female Lewis rats weighed 160 g-180 g were randomly divided into two
groups, EAMG group and CFA group. Rats in the EAMG group were immunized subcutaneously at the base of tail with 50ug AChR
R97-116 peptide in the final volume of 200 uL on day 0 and boosted on day30. The CFA group was immunized without the peptide
AChR R97-116. FACS was used to determine the expression of RAGE on CD4+T cell, ELISA was used to the expression of IFN-r, IL-4,
IL-17, TGF-beta, IL-6 and S100B in the supernatants of cultured lymphocytes, S100B was used to interfere the lymphocytes in vitro, the
effect of S100B on the proliferation, distribution of subtype and secretion of cytokines of T cells in EAMGA rats were further detected.Results:The expression of RAGE on CD4+T cells was higher in the EAMG group than that in the CFA group. The S100B concentration
in the serum was increased in the EAMG rats compared with the CFA rats (P< 0.001). S100B administration in vitro could cause
obviously higher Th1 and Th17 ratio and a lower Th2 and Treg ratio (PTh1<0.05，PTh17<0.05, PTh2> 0.05, PTreg<0.01) and increased the
AChR-specific T cell proliferation. The ELISA data showed that the concentration of IFN-r, IL-17 and IL-6 were increased, the level of
IL-4 and TGF-beta were decreased (PIFN-r<0.05, PIL-17 <0.05, PIL-6 <0.05, PTGF-beta<0.01, PIL-4 >0.05).Conclusion:RAGE and its ligand were
involved in the development of EAMG. S100B administrated in vitro could aggravate the disequilibrium of Th1, Th2, Th17 and Treg
subsets of CD4+ helper T cells and increased the AChR-specific T cell proliferation. |
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