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Expression of interferon inducible protein-10 in pancreas of mice 被引量:4

Expression of interferon inducible protein-10 in pancreas of mice
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摘要 AIM: To investigate the expression of interferon inducible protein-10 (IP-10) in pancreas of mice and to discuss its possible role in the pathogenesis of type 1 diabetes.METHODS: Non-obese diabetic (NOD) mice were used as experiment group and BALB/c mice as non-diabetic prone model. Immunohistochemistry method was used to evaluate the expression of IP-10 in the pancreas of NOD mice and BALB/c mice. Immunoelectron microscope was used to show the location of IP-10 in pancreatic islet β cells.RESULTS: Pancreatic islets were positively stained in all the NOD mice. Insulitis could be found in mice at the age of 4 wk. The weakly positive results were found in control group with no insulitis. Immunoelectron microscopy further demonstrated that IP-10 was produced by pancreatic β cells and stored in cytoplasm of the cells.CONCLUSION: IP-10 can be largely produced in pancreatic islets of NOD mice at the age of 2 wk when there is no significant insulitis, and may play an important part in the pathogenesis of type 1 diabetes by attracting immune cells to infiltrate the pancreatic islets. AIM: To investigate the expression of interferon inducible protein-10 (IP-10) in pancreas of mice and to discuss its possible role in the pathogenesis of type 1 diabetes. METHODS: Non-obese diabetic (NOD) mice were used as experiment group and BALB/c mice as non-diabetic prone model. Immunohistochemistry method was used to evaluate the expression of IP-10 in the pancreas of NOD mice and BALB/c mice. Immunoelectron microscope was used to show the location of IP-10 in pancreatic islet β cells. RESULTS: Pancreatic islets were positively stained in all the NOD mice. Insulitis could be found in mice at the age of 4 wk. The weakly positive results were found in control group with no insulitis. Immunoelectron microscopy further demonstrated that IP-10 was produced by pancreatic β cells and stored in cytoplasm of the cells. CONCLUSION: IP-10 can be largely produced in pancreatic islets of NOD mice at the age of 2 wk when there is no significant insulitis, and may play an important part in the pathogenesis of type 1 diabetes by attracting immune cells to infiltrate the pancreatic islets.
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第30期4750-4752,共3页 世界胃肠病学杂志(英文版)
关键词 Interferon inducible Protein-10 Type 1 diabetes INSULITIS 基因表达 干扰素诱导蛋白-10 胰岛疾病 1型糖尿病 细胞免疫
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  • 1Devendra D, Liu E, Eisenbarth GS. Type 1 diabetes: recent develovments. BMJ 2004; 328:750-754.
  • 2Atkinson MA, Eisenbarth GS. Type 1 diabetes: new perspectives on disease pathogenesis and treatment. LANCET 2001;358:221-229.
  • 3Atkinson MA, Wilson SB. Fatal attraction: chemokines and type 1 diabetes. J Clin Invest 2002; 110:1611-1613.
  • 4~,rimilli S, Ferlin W, Solvason N, Deshpande S, Howard M,Mocci S. Chemokines in autoimmune diseases. Immunol Rev 2000; 177:43-51.
  • 5Liu D, Cardozo AK, Darville MI, Eizirik DL. Double- stranded RNA cooperates with interferon-γ and IL-1β to induce both chemokine expression and nuclear factor-κB-dependent apoptosis in pancreatic β-cells: potential mechanisms for viral- induced insulitis and β-cell death in type 1 diabetes mellitus. Endocrinology 2002; 143:1225-1234.
  • 6Cardozo AK, Proost P, Gysemans C, Chen MC, Mathieu C,Eizirik DL. IL-1βand IFN-γinduce the expression of diverse chemokines and IL-15 in human and rat pancreatic islet cells,and in islets from pre-diabetic NOD mice. Diabetologia 2003;46:255-266.
  • 7Bradley LM, Asensio VC, Schioetz LK, Harbertson J, Krahl T, Patstone G, Woolf N, Campbell IL, Sarvetnick N. Isletspecific Thl, But Not Th2, cells secrete multiple chemokines and promote rapid induction of autoimmune diabetes. J Immunol 1999; 162:2511-2520.
  • 8Shimada A, Morimoto J, Kodama K, Suzuki R, Oikawa Y,Funae O, Kasuga A, Saruta T, Narumi S. Elevated serum IP-10 levels observed in type 1 diabetes. Diabetes Care 2001; 24:510-515.

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