کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3392363 | 1592683 | 2010 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IFN-γ and Fas/FasL pathways cooperate to induce medial cell loss and neointimal lesion formation in allograft vasculopathy
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: IFN-γ and Fas/FasL pathways cooperate to induce medial cell loss and neointimal lesion formation in allograft vasculopathy IFN-γ and Fas/FasL pathways cooperate to induce medial cell loss and neointimal lesion formation in allograft vasculopathy](/preview/png/3392363.png)
چکیده انگلیسی
We demonstrate that at 5-6 wk post transplantation in a wild type/wild type transplant CD8+ T cell infiltration, CD8+ CTL effector cell mediator expression and medial SMC loss all occur within aortic interposition grafts in the face of CNI immunosuppression. Both IFN-γ and CTL mediated effector function is required for SMC loss and lesion formation under these conditions. Using strain combinations and reconstitution models, we provide data that blockade of the perforin/granzyme pathway does not prevent lesion formation but that blockade of the Fas/FasL pathway of cytotoxicity dramatically reduces SMC loss and prevents neointimal lesion formation. Both of these blockade strategies are in the face of an active IFN-γ pathway. These data suggest a cooperative role between Fas/FasL and IFN-γ mediated effector functions in medial SMC loss and neointimal lesion formation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Transplant Immunology - Volume 22, Issues 3â4, February 2010, Pages 157-164
Journal: Transplant Immunology - Volume 22, Issues 3â4, February 2010, Pages 157-164
نویسندگان
Michael Hart-Matyas, Sara Nejat, Julie L. Jordan, Gregory M. Hirsch, Timothy D.G. Lee,