کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6161780 | 1249376 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CD11b is protective in complement-mediated immune complex glomerulonephritis
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای کلیوی
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چکیده انگلیسی
In chronic serum sickness, glomerular immune complexes form, yet C57BL/6 mice do not develop glomerulonephritis unless complement factor H (CfH) is absent, indicating the relevance of complement regulation. Complement receptor 3 (CD11b) and Fcγ receptors on leukocytes, and CfH on platelets, can bind immune complexes. Here we induced immune complex-mediated glomerulonephritis in CfHâ/â mice chimeric for wild-type, CfHâ/â, CD11bâ/â, or FcRγâ/â bone marrow stem cells. Glomerulonephritis was worse in CD11bâ/â chimeras compared with all others, whereas disease in FcRγâ/â and wild-type chimeras was comparable. Disease tracked strongly with humoral immune responses, but not glomerular immune complex deposits. Interstitial inflammation with M1 macrophages strongly correlated with glomerulonephritis scores. CD11bâ/â chimeras had significantly more M1 macrophages and CD4+ T cells. The renal dendritic cell populations originating from bone marrow-derived CD11c+ cells were similar in all experimental groups. CD11b+ cells bearing colony-stimulating factor 1 receptor were present in kidneys, including CD11bâ/â chimeras; these cells correlated negatively with glomerulonephritis scores. Thus, experimental immune complex-mediated glomerulonephritis is associated with accumulation of M1 macrophages and CD4+ T cells in kidneys and functional renal insufficiency. Hence, CD11b on mononuclear cells is instrumental in generating an anti-inflammatory response in the inflamed kidney.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Kidney International - Volume 87, Issue 5, May 2015, Pages 930-939
Journal: Kidney International - Volume 87, Issue 5, May 2015, Pages 930-939
نویسندگان
Jessy J. Alexander, Lee D. Chaves, Anthony Chang, Alexander Jacob, Maria Ritchie, Richard J. Quigg,