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趋化因子IP-10和MIP-3α在肝移植大鼠脾脏表达的研究

Expression of IP-10 and MIP-3α in rat spleen after liver transplantation
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摘要 目的 检测趋化因子IP—10和MIP-3α在肝移植大鼠脾脏的表达来研究二者在肝移植免疫中的作用。方法 建立大鼠肝移植模型,在移植后不同的时间点(3、5、7、10d)取脾脏标本,用免疫组织化学法检测IP—10和MIP-3α在脾脏的表达。结果 IP-10和MIP-3α主要在动脉周围淋巴鞘、边缘区、红髓的淋巴细胞和巨噬细胞表达。二者均于移植后第5天表达达高峰,两组间表达有显著性差异。结论 IP-10和MIP-3α在脾脏的表达有助于DC-T细胞接触,从而活化T细胞,进而诱发特异性免疫应答。 Objective To explore the immune effects of IP-10 and MIP-3α in rat liver, we detect the expression of IP-10 and MIP-3α in spleen at different time postoperatively.Methods Different rat allografi models were established. Acute liver allografi rejection groups: Wistar liver to SD rats; Control groups: SD liver to SD rats. Spleen samples were collected on clays 3,5, 7,10 postoperatively (each n = 3) . The expressions of IP-10 and MIP-3α in spleen were examined by means of im-munohistochemistry. Results The expression of IP-10 and MIP-3α in spleen was mainly in lymphocytes and macrophages in periarterial lymphatic sheaths , marginal zone and red pulp. The expression of IP-10 and MIP-3α reached a peak on days 5 postoperatively and had significantly difference in spleen between acute rejection groups and control groups. Conclusions The high expression of IP-10 and MIP-3α in spleen may be favor of DC processing antigen to naive T cells and activating T lymphocytes .
出处 《胃肠病学和肝病学杂志》 CAS 2004年第3期236-238,共3页 Chinese Journal of Gastroenterology and Hepatology
基金 北京大学985肝移植项目资助
关键词 趋化因子 IP-10 MIP-3Α 肝移植 大鼠 脾脏 T细胞 liver transplantation spleen chemokine IP-10 MIP-3α
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参考文献5

  • 1Zhang Z,Kaptanoglu L,Haddad W,et al.Donor T cell activation initiates small bowel allograft rejection through an IF-gamma-inducible protein-10-dependent mechanism.J Immunol,2002,168(7):3205-3212.
  • 2Wang C,Sun J,Wu L,et al.Antigen load and liver allograft survival.Transplant Proc,1998,31(1-2):455.
  • 3Wihelm M J,Pratschke J,Beato F,et al.Activation of the heart by donor brain death accelerated acute rejection after transplantation.Circulation,2000,102(19):2426-2433.
  • 4Dragun D,Hoff U,Park JK,et al.Prolonged cold preservation augments vascular injury independent of renal transplant immunogenicity and function.Kidney Int,2001,60(3):1773-1181.
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