Regulatory T Cells Contribute to the Recovery of Acute Lung Injury by Upregulating Tim-3
Regulatory T Cells Contribute to the Recovery of Acute Lung Injury by Upregulating Tim-3
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DOI：
10.1007/s10753-014-0096-7
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发表时间：
2015-06-01
期刊：
影响因子：
5.1
通讯作者：
Bai, Jianwen
中科院分区：
文献类型：
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作者：
Song, Haihan;Zhou, Yujia;Bai, Jianwen
急性肺损伤（acute lung injury，ALI）是一种以肺泡损伤和炎症失控为特征的疾病。ALI的发病机制尚不清楚。调节性T细胞（Regulatory T cells，Tcells），无论是天然的还是诱导的，抑制多种生理和病理免疫应答。在本研究中，我们调查了TdR是否参与了ALI的发展。采用流式细胞术检测66例ALI患者和30例健康对照者外周血中CD 4 + CD 25 + FoxP 3 + T细胞比例。结果表明，患者组T淋巴细胞占CD 4 + T细胞的比例（10.8%）明显高于对照组（7.6%）（P= 0.003）。此外，与研究期间死亡的患者相比，存活患者在招募时的TdR水平显著较高（P= 0.041）。由于Tim-3是一种负调控分子，可以调节Tcl 3的功能，我们评估了Tcl 3上的Tim-3水平，并确定了患者中该分子的上调。此外，与研究期间死亡的患者相比，存活的患者在招募时在Tclad上显示出1.7倍的Tim-3水平（P< 0.001）。这些结果表明，TIFE可能通过上调Tim-3的表达而影响ALI的预后。
Acute lung injury (ALI) is characterized by alveolar injury and uncontrolled inflammation. Mechanisms underlying pathogenesis of ALI are unknown. Regulatory T cells (Tregs), either natural or induced, suppress a variety of physiological and pathological immune responses. In the current study, we investigated whether Tregs were involved in the development of ALI. Proportion of CD4 + CD25 + FoxP3+ Tregs in the peripheral blood of 66 ALI patients and 30 healthy controls were examined by flow cytometry. Data showed that the percentage of Tregs in CD4+ T cells was significantly increased in patients than that in controls (10.8 versus 7.6%, P= 0.003). Also, compared to those who died during the study, patients who survived presented significantly higher level of Tregs at the time of recruitment (P= 0.041). Since Tim-3 is a negative regulatory molecule and can modulate the function of Tregs, we evaluated Tim-3 level on Tregs and identified upregulation of the molecule in patients than that in controls. Moreover, compared to those who died during the study, patients who survived showed 1.7-fold higher level of Tim-3 on Tregs at the time of recruitment (P< 0.001). These results suggest that Tregs could affect the prognosis of ALI probably due to the upregulation of Tim-3.