| 孔庆飞,张晓莉,朱 伟,王丹丹,谢晓丽,穆莉莉,么秀华,李呼伦.全反式维甲酸对乙酰胆碱受体特异性淋巴细胞的免疫调控作用[J].,2017,17(23):4426-4431 |
| 全反式维甲酸对乙酰胆碱受体特异性淋巴细胞的免疫调控作用 |
| The Immunomodulatory Effects of All-trans Retinoic Acid on AChR-specific Lymphocytes |
| 投稿时间：2017-01-19 修订日期：2017-02-13 |
| DOI：10.13241/j.cnki.pmb.2017.23.006 |
| 中文关键词: 全反式维甲酸 乙酰胆碱受体 重症肌无力 实验性自身免疫性重症肌无力 辅助性T细胞 |
| 英文关键词: All-trans retinoic acid Acetylcholine receptor Myasthenia Gravis Experimental Autoimmune Myasthenia Gravis T Helper cells |
| 基金项目:黑龙江省教育厅科学技术研究项目重点项目（12541z008） |
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| 中文摘要: |
| 摘要 目的：观察全反式维甲酸(ATRA)对乙酰胆碱受体(AChR)特异性淋巴细胞的体外调控作用，探讨其治疗重症肌无力(MG)的可能机制。方法：建立完全弗氏佐剂(CFA)对照组及实验性自身免疫性重症肌无力(EAMG)组大鼠，并获取淋巴结单个细胞悬液，以AChR97-116多肽片段以及不同浓度的ATRA体外培养72 h，采用流式细胞仪法、CCK-8法、ELISA法分别检测活细胞比例、细胞凋亡和周期的改变以及Th亚群的格局和B细胞抗体分泌能力的变化。结果：ATRA显著降低活细胞比例(P<0.001)；不同浓度的ATRA均促进了特异性细胞群的凋亡(P<0.001)，且呈剂量依赖性，而ATRA未改变AChR特异性淋巴细胞的生长周期；ATRA处理后，CFA和EAMG组的淋巴细胞增殖均受到明显抑制，且ATRA对AChR特异性的淋巴细胞的抑制明显(EAMG组，P<0.01)于CFA组(P<0.05)；ATRA干预后，AChR特异性CD4+T淋巴细胞的比例下降(P<0.01)，且ATRA促进了Th2、Treg细胞亚群百分比(P IL-4 <0.001，P Foxp3 <0.001)，而抑制了促炎性的Th17、Th1细胞亚群百分比(P IL-17 <0.05，P IFN-γ <0.001)；ATRA能够降低AChR特异性B细胞的抗体分泌能力(P<0.01)。结论：ATRA不仅能抑制AChR特异性T细胞功能，同时也能抑制AChR特异性B细胞功能，其在MG的临床治疗中可能起治疗作用。 |
| 英文摘要: |
| ABSTRACT Objective: To observe the effects of All-trans retinoic acid (ATRA) on the immune functions of AChR-specific lymph- cytes via in vitro assays, and investigate the possibility of ATRA in the clinical treatment of myasthenia gravis (MG). Methods: CFA con- trol group and EAMG experimental rats were established to obtain single lymphocytes suspension and cells were followed by AChR97-116 peptide with or without ATRA stimulation for 72 h, and then viable cell population, cell apoptosis, cell cycle and the distri- bution of Th cells were determined by flow cytometry. CCK-8 assay was selected to evaluate the effects of ATRA on proliferatory ability of lymphocytes. ELISA was used to detect the antibody secretion of B cells affected by ATRA. Results: Compared with CFA group, lym- phocytes obtained from EAMG rats had higher ratios of living cells, and this ratio was obviously decreased after ATRA treatment, P<0.001. Different concentrations of ATRA promoted the apoptosis of AChR-specific cells (P<0.001), and the promoted effects were ATRA dose-dependent, however, cell cycles were not changed. ATRA markedly inhibited the proliferation of cells from both CFA and EAMG groups, moreover, AChR-specific cells were more sensitive to ATRA treatment (P<0.01) than that of cells from CFA rats (P<0.05). The ratio of AChR-specific CD4+T cells was reduced by ATRA (P<0.01), and ATRA incubation significantly promoted the percentages of Th2, (P CD4+-IL-4+ <0.001), Treg (P CD4+-Foxp3+ <0.001) cell types, but markedly inhibited the percentages of Th17 (P CD4+-IL-17+ <0.05), Th1 (P CD4+- IFN-γ+ <0.001) cells. ELISA data showed us that ATRA obviously down regulated the antibody secretion of AChR-specific B cells, P<0.01. Conclusion: ATRA not only inhibited the functions of AChR-specific T cells, but also suppressed the roles of AChR-specific B cells, predicating a therapeutic effect of ATRA on myasthenia gravis therapy. |
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