کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956933 | 1099465 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotective effect of the immune system in a mouse model of severe dysmyelinating hereditary neuropathy: enhanced axonal degeneration following disruption of the RAG-1 gene
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
In mouse models of later onset forms of human hereditary demyelinating neuropathies, the immune system plays a crucial pathogenic role. Here, we investigated the influence of immune cells on early onset dysmyelination in mice homozygously deficient of the myelin component P0. In peripheral nerves of P0â/â mice, CD8+ T-lymphocytes increased with age. Macrophages peaked at 3 months followed by a substantial decline. They were mainly of hematogenous origin. To evaluate the functional role of immune cells, we cross-bred P0â/â mutants with RAG-1-deficient mice. At 3 months, the number of endoneurial macrophages did not differ from the macrophage number of immunocompetent myelin mutants, but the later decline of macrophages was not observed. Quantitative electron microscopy revealed that in plantar nerves of 6-month-old double mutants, significantly more axons had degenerated than in immunocompetent littermates. These data suggest a neuroprotective net effect of T-lymphocytes on axon survival in inherited, early onset dysmyelination.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 1, January 2005, Pages 118-127
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 1, January 2005, Pages 118-127
نویسندگان
Martin Berghoff, Mohtashem Samsam, Marcus Müller, Igor Kobsar, Klaus V. Toyka, Reinhard Kiefer, Mathias Mäurer, Rudolf Martini,