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Analysis of Pathogenesis of Autoimmune Insulitis in NOD Mice: Adoptive Transfer Experiments of Insulitis in ILI and NOD Nude Mice

机译:NOD小鼠自身免疫性岛炎的发病机制分析:ILI和NOD裸鼠的过继性胰岛素炎实验

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In an effort to study the pathophysiological events in the development of insulitis in NOD mice, we have developed ILI- and NOD-nuu mice. ILI mice are a nondiabetic inbred strain but are derived from the same Jcl:ICR mouse as NOD mice and share the same H-2 allotype with NOD mice. Splenocytes and CD4~+ cells from diabetic NOD mice appeared to transfer insulitis to ILI-nuu mice, suggesting that ILI mice already express autoantigen(s) responsible for insulitis. But reciprocal thymic grafts from NOD mice into ILI-nuu mice and those from ILI mice into NOD-nuu mice failed to allow the development of insulitis, implying that ILI mice possess neither precursor T cells nor the thymic environment responsible for the development of insulitis. In addition, splenocytes from ILI mice appeared to contain regulatory cells which suppress the development of diabetes but not that of insulitis in NOD mice. The use of these nude mice should provide more information on the products of insulitis-susceptibility genes of NOD mice.
机译:为了研究NOD小鼠胰岛炎发展中的病理生理事件,我们开发了ILI-和NOD-nu / nu小鼠。 ILI小鼠是非糖尿病近交系,但与NOD小鼠来自同一Jcl:ICR小鼠,与NOD小鼠具有相同的H-2同种异型。糖尿病NOD小鼠的脾细胞和CD4〜+细胞似乎将胰岛素炎转移至ILI-nu / nu小鼠,这表明ILI小鼠已经表达了引起胰岛素炎的自身抗原。但是,从NOD小鼠到ILI-nu / nu小鼠的相互胸腺移植物以及从ILI小鼠到NOD-nu / nu小鼠的相互胸腺移植物均不能使胰岛炎发展,这意味着ILI小鼠既不具有前体T细胞,也不具有负责该过程的胸腺环境。胰岛炎的发展。此外,ILI小鼠的脾细胞似乎含有调节性细胞,可抑制NOD小鼠中糖尿病的发展,但不能抑制胰岛炎的发展。这些裸鼠的使用应提供有关NOD鼠对胰岛素炎敏感性基因产物的更多信息。

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