Bacille Calmette-Guerin/DNAhsp65 prime-boost is protective against diabetes in non-obese diabetic mice but not in the streptozotocin model of type 1 diabetes

Bacille Calmette-Guerin/DNAhsp65 prime-boost is protective against diabetes in non-obese diabetic mice but not in the streptozotocin model of type 1 diabetes
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DOI:
10.1111/cei.12140
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发表时间:
2013-09-01
影响因子:
4.6
通讯作者:
Sartori, A.
Sartori, A.
中科院分区:
医学3区
文献类型:
--
作者:
daRosa, L. C.;Chiuso-Minicucci, F.;Sartori, A.

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I型糖尿病是一种由胰腺中β细胞的自身免疫破坏引起的疾病,其导致胰岛素产生不足。本研究的目的是评估包括卡介苗(BCG)和pVAXhsp 65疫苗(BCG/DNAhsp 65)的初免-加强策略在链脲佐菌素(STZ)诱导的C57 BL/6小鼠糖尿病和非肥胖糖尿病(NOD)小鼠自发性1型糖尿病中的预防潜力。与未免疫的NOD小鼠相比,NOD小鼠中的BCG/DNAhsp 65疫苗接种确定了体重增加、针对高血糖症的保护、胰岛炎症减少、脾脏细胞因子产生水平更高以及脾脏中调节性T细胞数量减少。然而,在STZ模型中,临床参数没有显著差异。虽然这种疫苗接种策略在STZ模型中不能保护小鼠,但在NOD小鼠中非常有效。这是第一份报告表明,初免-加强策略可以作为一种免疫调节程序在自身免疫性疾病中进行探索。
Type I diabetes is a disease caused by autoimmune destruction of the beta cells in the pancreas that leads to a deficiency in insulin production. The aim of this study was to evaluate the prophylactic potential of a prime-boost strategy involving bacille Calmette-Guerin (BCG) and the pVAXhsp65 vaccine (BCG/DNAhsp65) in diabetes induced by streptozotocin (STZ) in C57BL/6 mice and also in spontaneous type 1 diabetes in non-obese diabetic (NOD) mice. BCG/DNAhsp65 vaccination in NOD mice determined weight gain, protection against hyperglycaemia, decreased islet inflammation, higher levels of cytokine production by the spleen and a reduced number of regulatory T cells in the spleen compared with non-immunized NOD mice. In the STZ model, however, there was no significant difference in the clinical parameters. Although this vaccination strategy did not protect mice in the STZ model, it was very effective in NOD mice. This is the first report demonstrating that a prime-boost strategy could be explored as an immunomodulatory procedure in autoimmune diseases.