期刊文献+

融合蛋白HSP65-6×P277在NOD鼠中降糖作用的机制研究(英文)

Study on the hypoglycemic mechanism of the fusion protein HSP65-6×P277 in NOD mice
下载PDF
导出
摘要 目的:探讨融合蛋白HSP65 -6×P277在NOD鼠中的降糖作用机制。方法:融合蛋白HSP65 -6×P277通过鼻腔给药方式,在不添加任何佐剂的情况下3次免疫4周龄雌性NOD小鼠。观察该融合蛋白对NOD小鼠血糖,细胞因子水平,抗体类型和胰腺炎严重程度的影响。结果:融合蛋白HSP65 -6×P277免疫组动物血清中含有高水平的IL-4和低水平的IL-2 ,P277特异性抗体类型主要为IgGl和IgG2b,IgG2a水平较低;T细胞增殖实验的培养上清中含有较高水平的IL-10和较低水平的IFN-γ;胰腺炎的严重程度和1型糖尿病的发病率显著降低。结论:诱导了Th2免疫反应可能是HSP65-6×P277预防1型糖尿病发生的作用机制之一。 AIM:To evaluate the hypoglycemic mechanism of the fusion protein HSP65-6×P277 in NOD mice.METHODS:The fusion protein was used to immunize 4-week old female NOD mice with three i.n.inoculations in the absence of adjuvants.The effects of HSP65-6×P277 on NOD mice were investigated by observing the change of blood glucose,cytokine levels,antibody types and degree of insulitis.RESULTS:The sera collected from HSP65-6×P277 treated mice,contained relatively high levels of interleukin IL-4 but low levels of IL-2,and the antibody types were almost exclusively of the IgGl and IgG2b subclass,but at very low levels of IgG2a.T cells from HSP65-6×P277 treated mice when incubated with HSP-peptide conjugate showed an increase in IL-10 secretion and a decrease in interferon (IFN)-γ secretion.HSP65-6×P277 treatment reduced insulitis and T1DM incidence.CONCLUSION:The hypoglycemic mechanism of the fusion protein HSP65-6×P277 is related to its inducing Th2 responses.
出处 《中国临床药理学与治疗学》 CAS CSCD 2009年第10期1142-1150,共9页 Chinese Journal of Clinical Pharmacology and Therapeutics
基金 supported by China National Natural Science Fund Commit-tee(Grant No.30701023,30672464 and 30500458)
关键词 热休克蛋白65 p277肽 TH1/TH2细胞 细胞因子 heat shock protein 65 P277 Th1/Th2 cells cytokines
  • 相关文献

参考文献48

  • 1yon Herrath MG. Pathogenesis of type 1 diabetes: a viewpoint[J]. Adv Exp Med Biol, 2004,552(2) :317 - 321.
  • 2Denis D. Type 1 diabetes[J]. Lancet, 2006,367(9513) : 847 - 858.
  • 3Miller BJ, Appel MC, O' Neill JJ, et al. Both the Lyt2 + and 1.3T4 + T cell subsets are required for the transfer of diabetes in nonobeses diabetic mice [ J ]. J Inununol, 1988,140(1) :52 - 58.
  • 4Christianson SW, Schultz LD, Leiter ED. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice. Relative contributions of CD4 ^+ and CD8^+ T cells from diabetic versus prediabetic NOD. NON-Thy-1a donors[J] . Diabetes, 1993,42(1) :44- 55.
  • 5Soderstrom I, Bergman ML, Colussi F, et al. Establishment and characterization of RAG-2 deficient non-obese diabetic mice[J]. Scand J Immunol, 1996, 43 (3) : 525 - 530.
  • 6Christianson SW, Shuhz LD, Leiter EH. Adoptive transfer of diabetes into immunodeficient NOD-scid/scid mice: relative contributions of CD4^+ and CD8^ + T cells from diabetic versus prediabetic NOD. NOD-Thy-la donors [J]. Diabetes, 1993,42(1) :44- 55.
  • 7Mosmann TR, Coffman RL. Two types of mouse helper T cell clone: implications for immune regulation[ J]. Immunol, Today, 1987,8 (7) : 223 - 227.
  • 8Mosmann TR, Coffiman RL. TH1 and TH2 cells, different patterns of lymphokine secretion lead to different functional properties[J]. Ann Rev Immunol, 1989, 7 (7): 145 - 173.
  • 9Abbas AK, Murphy KM, Sher A. Functional diversity of helper lymphocytes[J]. Nature (Lond), 1996,383(11) : 787 - 793.
  • 10Trembleau S, Penna G, Bosi E, et al. Interleukin 12 administration induces T helper type 1 cells and accelerates autoimmune diabetes[J]. J Exp Med, 1995, 181(2) : 817 - 821.

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