Is innervation an early target in autoimmune diabetes?
In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are...
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2003
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714906_v24_n11_p574_Saravia http://hdl.handle.net/20.500.12110/paper_14714906_v24_n11_p574_Saravia |
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paper:paper_14714906_v24_n11_p574_Saravia |
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paper:paper_14714906_v24_n11_p574_Saravia2023-06-08T16:17:21Z Is innervation an early target in autoimmune diabetes? autoantigen chemokine cytokine glucose 6 phosphatase glutamate decarboxylase growth factor isoenzyme protein subunit autoimmune disease catalysis cell differentiation environmental factor enzyme activity genetic polymorphism genetics human insulin dependent diabetes mellitus lymphocyte multigene family nerve cell nervous system non insulin dependent diabetes mellitus nonhuman organogenesis pancreas islet beta cell protein expression review In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are involved in phagocytosis of apoptotic neurons. Pertinently, MΦ are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient β-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis. 2003 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714906_v24_n11_p574_Saravia http://hdl.handle.net/20.500.12110/paper_14714906_v24_n11_p574_Saravia |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
autoantigen chemokine cytokine glucose 6 phosphatase glutamate decarboxylase growth factor isoenzyme protein subunit autoimmune disease catalysis cell differentiation environmental factor enzyme activity genetic polymorphism genetics human insulin dependent diabetes mellitus lymphocyte multigene family nerve cell nervous system non insulin dependent diabetes mellitus nonhuman organogenesis pancreas islet beta cell protein expression review |
| spellingShingle |
autoantigen chemokine cytokine glucose 6 phosphatase glutamate decarboxylase growth factor isoenzyme protein subunit autoimmune disease catalysis cell differentiation environmental factor enzyme activity genetic polymorphism genetics human insulin dependent diabetes mellitus lymphocyte multigene family nerve cell nervous system non insulin dependent diabetes mellitus nonhuman organogenesis pancreas islet beta cell protein expression review Is innervation an early target in autoimmune diabetes? |
| topic_facet |
autoantigen chemokine cytokine glucose 6 phosphatase glutamate decarboxylase growth factor isoenzyme protein subunit autoimmune disease catalysis cell differentiation environmental factor enzyme activity genetic polymorphism genetics human insulin dependent diabetes mellitus lymphocyte multigene family nerve cell nervous system non insulin dependent diabetes mellitus nonhuman organogenesis pancreas islet beta cell protein expression review |
| description |
In the non-obese diabetic (NOD) mouse, a spontaneous model of type 1 diabetes (T1D), recent evidence suggests that Schwann cells (Scs) and neurons surrounding insulin-producing β cells of the islets of Langerhans are destroyed before β cells. During normal perinatal development, macrophages (MΦ) are involved in phagocytosis of apoptotic neurons. Pertinently, MΦ are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient β-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis. |
| title |
Is innervation an early target in autoimmune diabetes? |
| title_short |
Is innervation an early target in autoimmune diabetes? |
| title_full |
Is innervation an early target in autoimmune diabetes? |
| title_fullStr |
Is innervation an early target in autoimmune diabetes? |
| title_full_unstemmed |
Is innervation an early target in autoimmune diabetes? |
| title_sort |
is innervation an early target in autoimmune diabetes? |
| publishDate |
2003 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_14714906_v24_n11_p574_Saravia http://hdl.handle.net/20.500.12110/paper_14714906_v24_n11_p574_Saravia |
| _version_ |
1768546132068139008 |