期刊文献+

骨髓基质干细胞治疗实验性自身免疫性神经炎的研究 被引量:2

Study on therapy of experimental autoimmune neuritis by bone marrow stromal cells
下载PDF
导出
摘要 目的:探讨骨髓基质干细胞(BMSC)移植治疗实验性自身免疫性神经炎(experimentalautoimmuneneuritis,EAN)的疗效以及相应的作用机制。方法:用P0180-199多肽与弗氏完全佐剂的混合液免疫Lewis大鼠,建立EAN动物模型。治疗组在免疫后第10天,尾静脉回输荧光染料PKH26标记的BMSC(2×106个细胞/只),通过临床评估、免疫组化及ELISA等方法,研究了BMSC对EAN的治疗作用。结果:回输的BMSC能向脱髓鞘神经组织周围迁移,减轻脱髓鞘的病理改变和炎性细胞浸润。与对照组比较,治疗组CD4+和CD8+T细胞的浸润显著减少(P<0.05),血清中IFN-γ和TNF-α的水平明显降低(P<0.05),培养上清中IL-4的水平显著增加(P<0.05)。结论:BMSC静脉移植治疗EAN有一定的疗效。BMSC通过调节细胞因子的表达逆转Th1/Th2型细胞之间的失衡而发挥治疗作用,并能够抑制T细胞活化增殖。 AIM: To investigate the therapeutic effect of bone marrow stromal cells (BMSCs) transplantation on experimental autoimmune neuritis (EAN) and study the possible mechanism. METHODS: EAN model was established by immunizing Lewis rats with Po180-199 peptide and complete Freund's adjuvant (CFA). In the therapy group, BMSCs (2 × 10^6 cells/rat) were marked with fluorochrome PKH26 and injected into the rats' caudal vein 10 d after immunization. The therapeutic effect of BMSC transplantation on EAN rats was investigated by clinical assessment, immunohistochemical staining, and ELISA, respectively. RESULTS: The injected BMSCs could migrate to the demyelinated nerve tissues, and the demyelination and inflammatory ir, filtration was relieved. The infiltration of CD4^+ and CD8^+ T cells and the sera level of IFN-γ and TNF-α were decreased significantly( P 〈0.05), whereas IL-4 level in the supernatant of cultured lymphocytes was increased ( P 〈 0. 05 ). CONCLUSION: Certain therapeutic effect of BMSC transplantation on EAN was observed. BMSCs could reverse the disbalance of Th1/Th2 cells by regulating the cytokine expression and could inhibit the activation and proliferation of T cells.
出处 《细胞与分子免疫学杂志》 CAS CSCD 北大核心 2007年第1期52-55,共4页 Chinese Journal of Cellular and Molecular Immunology
基金 国家"十五"科技攻关计划引导项目(2004DA754C) 黑龙江省卫生厅科技攻关项目(2005-29)
  • 相关文献

参考文献10

  • 1Kehoe M.Guillain-Barre syndrome-a patient guide and nursing resource[J].Axone,2001,22(4):16-24. 被引量:1
  • 2Bao L,Lindgren JU,van der Meide P,et al.The critical role of IL-12 p40 in initiating,enhancing,and perpetuating pathogenic events in murine experimental autoimmune neuritis[J].Brain Pathol,2002,12(4):420-429. 被引量:1
  • 3Barry FP.Biology and clinical applications of mesenchymal stem cells[J].Birth Defects Res C Embryo Today,2003,69(3):250-256. 被引量:1
  • 4Cavaletti G,Mata S,Fasano A,et al.Lipid-free versus lipid-bound P2 protein-induced experimental allergic neuritis:clinicopathological,neurophysiological,and immunological study[J].J Neurosci Res,2000,62(5):709-716. 被引量:1
  • 5Dezawa M,Kanno H,Hoshino M,et al.Specific induction of neuronal cells from bone marrow stromal cells and application for autologous transplantation[J].J Clin Invest,2004,113(12):1701-1710. 被引量:1
  • 6Munoz-Elias G,Marcus AJ,Coyne TM,et al.Adult bone marrow stromal cells in the embryonic brain:engraftment,migration,differentiation,and long-term survival[J].J Neurosci,2004,24(19):4585-4595. 被引量:1
  • 7Di Nicola M,Carlo-Stella C,Magni M,et al.Human bone marrow stromal cells suppress T-lymphocyte proliferation induced by cellular or nonspecific mitogenic stimuli[J].Blood,2002,99(10):3838-3843. 被引量:1
  • 8宣旻,邱国强,谢晓宝.间充质干细胞对混合淋巴细胞反应体系中T淋巴细胞的免疫调节作用[J].细胞与分子免疫学杂志,2006,22(4):433-435. 被引量:7
  • 9Krampera M,Glennie S,Dyson J,et al.Bone marrow mesenchymal stem cells inhibit the response of naive andmemory antigen-specific T cells to their cognate peptide[J].Blood,2003,101(9):3722-3729. 被引量:1
  • 10方伟,刘洪波,方树友,周媛.格林-巴利综合征患者血清IFN-γ、IL-4水平及意义[J].实用神经疾病杂志,2005,8(1):2-4. 被引量:1

二级参考文献27

  • 1[1]Dahle C, Vrethem M, Ernrudh J. T lymphocyte subset abnormalitives in peripheral blood from patients GBS,J Neurimmu,1994,53:219 被引量:1
  • 2[2]Asbury AK, Cornblath DR. Assessment of current diagnostic criteria for GBS. Ann Neurol,1990,27:21 被引量:1
  • 3[3]Hughes RAC, Newson-davis J, Verkin G, et al. Controlled trial ofpredxisolone in acute polyneuropathy.Lancet,1978,2:750 被引量:1
  • 4[4]Poser CM. The diagnosis of multiple sclerosis. Thieme-Stration Inc.New York,1984. 被引量:1
  • 5[5]Hughes RAC. Immunological mechanisms of demyelination.J R SocMed,1992,85:53 被引量:1
  • 6[6]Romagnani S.(review) Biology of Human Th1 and Th2 Cell J Ciln Immun,1995,15(3):121 被引量:1
  • 7[7]Schmidt B, Stoll G, Vander Meide,et al.Transient cellular expression of interferon-gamma in myelin-induced and T cell line-mediated experimental autoimmune neuritis. Brain,1992(in press) 被引量:1
  • 8[8]Strigand K, Holmdahl R,Vander Meide. In vivo treatment of rats with monoclonal antibodies against gamma interferon:effects on experimental allergic neuritis. Acta Neurol Scand,1989,80:201 被引量:1
  • 9[9]Racke MK, Bonomo A, Scott DE, et al. Cytokine-induced immune deviation as a therapy for inflammatory autoimmune disease.J Exp Med,1994,19:61 被引量:1
  • 10[10]Tsai CP, Pollard JD and Armati PJ. Interferon-γ inhibition suppresses exprimental allergic neuritis:modulation of major histocompatibility complex expression on Schwann cells in vitro.J Neuroimmu,1992,31:133 被引量:1

共引文献6

同被引文献13

引证文献2

二级引证文献2

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部