کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3368368 | 1218785 | 2008 | 7 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: GM-CSF-induced autoimmune gastritis in interferon α receptor deficient mice GM-CSF-induced autoimmune gastritis in interferon α receptor deficient mice](/preview/png/3368368.png)
Experimental autoimmune gastritis (EAG), a mouse model of human autoimmune gastritis, is characterised by gastric mononuclear cell infiltrates and parietal and zymogenic cell destruction. The gastritis is accompanied by circulating auto-antibodies to parietal cell-associated gastric H+/K+ ATPase. As interferon α has been implicated in the regulation of immune responses, we asked whether EAG induced by the local transgenic expression of granulocyte-macrophage colony stimulating factor (GM-CSF) in the stomach (PC-GMCSF transgenic mice) would be affected by deficiency of its binding receptor. To address this, we crossed PC-GMCSF transgenic mice with mice deficient in interferon α (IFNα) receptor2 (IFNAR2). We found that EAG development in the PC-GMCSF transgenic mice was not affected by IFNAR2 deficiency. There was no difference in severity of gastric pathology, nor in autoantibody levels in the IFNAR2 deficient mice compared to wild-type, and heterozygous littermates. We conclude that the local transgenic expression of GM-CSF in the stomach overrides any possible modulatory effects of IFNAR2 on EAG development.
Journal: Journal of Autoimmunity - Volume 31, Issue 3, November 2008, Pages 274–280