کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9194565 | 1580504 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Retinal degeneration in experimental coronavirus retinopathy (ECOR) is associated with increased TNF-α, soluble TNFR2 and altered TNF-α signaling
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
ایمونولوژی
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چکیده انگلیسی
Experimental coronavirus retinopathy (ECOR) is a virally triggered model of retinal degeneration composed of both genetic and autoimmune components. Since TNF-α plays a role in immune-mediated processes we evaluated the levels of TNF-α/TNF-α receptors and the downstream signaling molecule nitric oxide (NO) during disease in both retinal degeneration susceptible BALB/c and degeneration resistant CD-1 mice. Following coronavirus injection, TNF-α mRNA was detected at higher levels within the retinas, and concentrations of TNF-α (p < 0.005) and sTNFR1 (p < 0.0005) proteins were increased within the sera of BALB/c but not CD-1 mice. While concentrations of sTNFR2 proteins were elevated in both BALB/c (p < 0.00005) and CD-1 (p < 0.005) mice compared to controls, concentrations were higher in BALB/c mice (p < 0.0005). Gene expression of iNOS while initially high in BALB/c mice decreased during the acute phase of infection, while it increased in CD-1 mice. These trends are attributable to differences in monocyte TNFR2 release (p < 0.0005) between the strains since sTNFR2 decreased (p < 0.01) levels of NO production. These studies demonstrate that retinal degeneration following viral infection is associated with increased release of TNF-α/TNF receptors combined with a down-regulation of NO. Furthermore they suggest that these molecules are involved in alterations in immune response leading to autoimmune reactivity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Neuroimmunology - Volume 166, Issues 1â2, September 2005, Pages 65-74
Journal: Journal of Neuroimmunology - Volume 166, Issues 1â2, September 2005, Pages 65-74
نویسندگان
Laura C. Hooper, Marian S. Chin, Barbara Detrick, John J. Hooks,