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首页> 外文期刊>Life sciences >Induction of virus-induced IDDM in virus resistant mice without lymphocyte maturation.
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Induction of virus-induced IDDM in virus resistant mice without lymphocyte maturation.

机译：在没有淋巴细胞成熟的病毒抗性小鼠中诱导病毒诱导的IDDM。

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摘要

The role of lymphocytes in the pathogenesis of viral-induced insulin dependent diabetes mellitus (IDDM) is controversial. To better understand how a virus-induced IDDM depends on the infiltrating lymphocytes, encephalomyocarditis virus (EMCV) was inoculated intraperitoneally into three kinds of mice; virus-susceptible C57BL/6, virus-resistant 129/SV and recombination activity gene-2 (Rag2) knockout 129/SV mice. Pancreatic inflammation and beta cell necrosis were evaluated after EMCV, D variant (10(3) pfu/mouse) inoculation. On post-inoculation day 14, the lethal rates of C57BL/6, 129/SV and Rag2 knockout mice were 52, 10 and 100%, respectively. The blood glucose in Rag2KO mice on day 8 was significantly elevated as compared with 129SV mice (231 +/- 49 vs 169 +/- 32 mg/dl, P<0.05). In situ hybridization demonstrated the EMCV genome in the pancreas of Rag2 knockout and C57BL/6 mice, but not in 129/SV mice. Beta cell necrosis were more severe in Rag-2 knockout mice than in wild type 129/SV mice, but lymphocyte infiltration was less severe than C57BL/6. Pancreas in Rag2 knockout mice infected with virus were affected more severely than the virus-resistant strain of mice. Diabetogenic virus induced IDDM in virus-resistant mice without mature lymphocytes.
机译：淋巴细胞在病毒性胰岛素依赖型糖尿病（IDDM）发病机理中的作用是有争议的。为了更好地了解病毒诱导的IDDM如何依赖于浸润的淋巴细胞，将脑心肌炎病毒（EMCV）腹膜内接种到三种小鼠中。易感病毒C57BL / 6，抗病毒129 / SV和重组活性基因2（Rag2）敲除129 / SV小鼠。接种EMCV，D变体（10（3）pfu /小鼠）后评估胰腺炎症和β细胞坏死。接种后第14天，C57BL / 6、129 / SV和Rag2基因敲除小鼠的致死率分别为52％，10％和100％。与129SV小鼠相比，第8天Rag2KO小鼠的血糖显着升高（231 +/- 49对169 +/- 32 mg / dl，P <0.05）。原位杂交表明，Rag2基因敲除小鼠和C57BL / 6小鼠的胰腺中有EMCV基因组，而129 / SV小鼠中没有。与野生型129 / SV小鼠相比，Rag-2基因敲除小鼠的β细胞坏死更为严重，但淋巴细胞浸润的程度不及C57BL / 6。与病毒抗性品系相比，感染病毒的Rag2基因敲除小鼠的胰腺受到的影响更大。在没有成熟淋巴细胞的抗病毒小鼠中，糖尿病病毒诱导了IDDM。

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