Diabetic ketoacidosis induces in vivo activation of human T-lymphocytes
Diabetic ketoacidosis induces in vivo activation of human T-lymphocytes
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DOI：
10.1016/j.bbrc.2004.01.065
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发表时间：
2004-03-05
影响因子：
3.1
通讯作者：
Umpierrez, GE
中科院分区：
文献类型：
--
作者：
Kitabchi, AE;Stentz, FB;Umpierrez, GE
糖尿病酮症酸中毒(DKA)是一种与中性粒细胞(PMN)免疫反应相关的炎症状态。然而，DKA患者PMN中T淋巴细胞亚群的激活尚不清楚。我们通过检测8例患者入院时和DKA缓解时的胰岛素、IGF-1和IL-2的从头生长因子受体，研究了CD4和CD8淋巴细胞的活体激活，并与匹配的对照组进行了比较。这些受体在入院时在所有患者的淋巴细胞中都存在，但在对照组中没有。这一事件与硫代巴比妥酸反应物质和二氯荧光素水平升高有关，它们是氧化应激的标志。基于这些新的发现和文献中的工作，我们假设高血糖/酮症会导致活性氧的增加，导致细胞因子水平的增加和生长因子受体的出现。我们认为DKA将T淋巴细胞转化为对胰岛素敏感的组织作为一种代偿机制。(C)2004 Elsevier Inc.保留所有权利。
Diabetic ketoacidosis (DKA) is an inflammatory state associated with immune responses in polymorphonuclear cells (PMN). Activation of subgroup of T-lymphocytes in PMN of DKA patients, however, is not known. We studied in vivo activation of CD4 and CD8 lymphocytes by measuring de novo growth factor receptor for insulin, IGF-1, and IL-2 in eight patients on admission and at resolution of DKA, and compared them with matched controls. The presence of these receptors was demonstrated in all patients' lymphocytes on admission, but not in control subjects. This event was associated with increased levels of thiobarbituric acid-reacting material and dichlorofluorescien, as markers of oxidative stress. Based on these new findings and works in the literature, we hypothesize that hyperglycemia/ketosis results in increased reactive oxygen species, leading to increased levels of cytokines and emergence of growth factor receptors. We propose DKA changes the T-lymphocytes to insulin sensitive tissues as a compensatory mechanism. (C) 2004 Elsevier Inc. All rights reserved.