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首页> 外文期刊>Journal of Cellular Physiology >Protective effects of carbonyl iron against multiple low‐dose streptozotocin‐induced diabetes in rodents
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Protective effects of carbonyl iron against multiple low‐dose streptozotocin‐induced diabetes in rodents

机译:羰基铁对保护的影响多种低剂量链脲霉素诱导糖尿病应承担的在啮齿动物

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Particulate adjuvants have shown increasing promise as effective, safe, and durable agents for the stimulation of immunity, or alternatively, the suppression of autoimmunity. Here we examined the potential of the adjuvant carbonyl iron (CI) for the modulation of organ‐specific autoimmune disease—type 1 diabetes (T1D). T1D was induced by multiple low doses of streptozotocin (MLDS) that initiates beta cell death and triggers immune cell infiltration into the pancreatic islets. The results of this study indicate that the single in vivo application of CI to MLDS‐treated DA rats, CBA/H mice, or C57BL/6 mice successfully counteracted the development of insulitis and hyperglycemia. The protective action was obtained either when CI was applied 7 days before, simultaneously with the first dose of streptozotocin, or 1 day after MLDS treatment. Ex vivo cell analysis of C57BL/6 mice showed that CI treatment reduced the proportion of proinflammatory F4/80 + CD40 + M1 macrophages and activated T lymphocytes in the spleen. Moreover, the treatment down‐regulated the number of inflammatory CD4 + IFN‐γ + cells in pancreatic lymph nodes, Peyer's patches, and pancreas‐infiltrating mononuclear cells, while simultaneously potentiating proportion of CD4 + IL17 + cells. The regulatory arm of the immune system represented by CD3 + NK1.1 + (NKT) and CD4 + CD25 + FoxP3 + regulatory T cells was potentiated after CI treatment. In vitro analysis showed that CI down‐regulated CD40 and CD80 expression on dendritic cells thus probably interfering with their antigen‐presenting ability. In conclusion, particulate adjuvant CI seems to suppress the activation of the innate immune response, which further affects the adaptive immune response directed toward pancreatic beta cells.
机译:微粒佐剂显示增加承诺是有效、安全、耐用刺激免疫力,或另外,自身免疫的抑制。我们检查辅助的潜力羰基铁(CI)的调制1地理器官自身免疫性disease-type糖尿病(近年来)。链脲霉素(MLDS)启动β细胞死亡和触发免疫细胞浸润胰岛细胞。表明,单一体内应用CI地理MLDS DA大鼠治疗,CBA / H老鼠,或者C57BL / 6小鼠成功抵消了胰岛炎和高血糖的发展。保护行动要么CI时获得的应用前7天,同时用第一剂量链脲霉素或MLDS后1天治疗。表明,CI治疗比例减少的促炎F4/80 + CD40 + M1巨噬细胞并激活T淋巴细胞在脾脏。此外,治疗量监管的数量炎症的CD4 +干扰素γ+细胞在胰腺淋巴结、派尔集合淋巴结补丁胰腺高浸润的单核细胞同时其余的CD4 +比例IL17 +细胞。系统由CD3 + NK1.1 + (NKT)和CD4细胞+ CD25 + FoxP3 +调节性T细胞CI治疗后疗效。表明,CI应承担监管CD40 CD80树突状细胞上的表达从而可能干扰他们的抗原呈递能力。似乎抑制先天的激活免疫反应,进而影响针对自适应免疫反应胰腺β细胞。

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