Is innervation an early target in autoimmune diabetes?
Is innervation an early target in autoimmune diabetes?
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DOI：
10.1016/j.it.2003.09.010
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发表时间：
2003-11-01
影响因子：
16.8
通讯作者：
Homo-Delarche, F
中科院分区：
文献类型：
--
作者：
Saravia, F;Homo-Delarche, F
在非肥胖糖尿病（NOD）小鼠中，1型糖尿病（T1D）的自发模型，最近的证据表明，雪旺细胞（Scs）和胰岛的胰岛素产生β细胞周围的神经元在β细胞之前被破坏。在正常的围产期发育过程中，巨噬细胞（MPhi）参与吞噬凋亡神经元。相关地，MPhi在出生时就已经存在于NOD胰腺中。他们可能异常控制的神经吞噬作用，连同短暂的β细胞过度活跃和淋巴细胞异常，可能共同参与T1D的发病机制。
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 beta cells of the islets of Langerhans are destroyed before beta cells. During normal perinatal development, macrophages (MPhi) are involved in phagocytosis of apoptotic neurons. Pertinently, MPhi are already present at birth in NOD pancreata. Their possible abnormal control of nerve phagocytosis, together with transient beta-cell hyperactivity and lymphocyte anomalies, might conjointly participate in T1D pathogenesis.