The relationship between CD4+CD25+CD127- regulatory T cells and inflammatory response and outcome during shock states.
The relationship between CD4+CD25+CD127- regulatory T cells and inflammatory response and outcome during shock states.
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DOI：
10.1186/cc8876
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Gibot S
中科院分区：
文献类型：
--
作者：
Hein F;Massin F;Cravoisy-Popovic A;Barraud D;Levy B;Bollaert PE;Gibot S
虽然调节性T淋巴细胞（Tlymphocyte，Tlymphocyte）在预防自身免疫性疾病和限制慢性炎症性疾病方面具有关键作用，但它们也可能通过阻止对某些病原体的杀菌免疫来阻断有益的免疫应答。为了确定天然存在的Treg细胞是否在休克状态下的炎症反应和结果中起作用，我们在一所大学医院的两个成人ICU中进行了一项观察性研究。在入院12小时内，采集外周全血用于细胞因子的测量和淋巴细胞计数的测定。在第三、五和七天重复取样。此外，通过盲肠结扎和穿孔在成年Balb/c小鼠中诱导实验性感染性休克。纳入43例休克患者（26例脓毒性，17例非脓毒性）和7例健康志愿者。休克发生后3天，THBE的百分比增加，但其绝对数量仍低于健康志愿者。在感染和非感染患者中发现了类似的TcR动力学模式。虽然严重程度评分和THBE百分比之间呈负相关，但THBE的时间进程在幸存者和非幸存者之间相似。在脓毒症小鼠中，虽然脾细胞中Treg细胞亚群迅速增加，但脓毒症发作前抗体诱导的Tcl 3耗竭并不改变存活率。这些数据反驳了休克状态下TdR在炎症反应和结局中的决定性作用。
Although regulatory T lymphocytes (Tregs) have a pivotal role in preventing autoimmune diseases and limiting chronic inflammatory conditions, they may also block beneficial immune responses by preventing sterilizing immunity to certain pathogens. To determine whether naturally occurring Treg cells have a role in inflammatory response and outcome during shock state we conducted an observational study in two adult ICUs from a university hospital. Within 12 hours of admission, peripheral whole blood was collected for the measurement of cytokines and determination of lymphocyte count. Sampling was repeated at day three, five and seven. Furthermore, an experimental septic shock was induced in adult Balb/c mice through caecal ligation and puncture. Forty-three patients suffering from shock (26 septic, 17 non septic), and 7 healthy volunteers were included. The percentage of Tregs increased as early as 3 days after the onset of shock, while their absolute number remained lower than in healthy volunteers. A similar pattern of Tregs kinetics was found in infected and non infected patients. Though there was an inverse correlation between severity scores and Tregs percentage, the time course of Tregs was similar between survivors and non survivors. No relation between Tregs and cytokine concentration was found. In septic mice, although there was a rapid increase in Treg cells subset among splenocytes, antibody-induced depletion of Tregs before the onset of sepsis did not alter survival. These data argue against a determinant role of Tregs in inflammatory response and outcome during shock states.
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