中文摘要：

目的探讨严重烧伤患者T细胞免疫功能的变化规律及其与高迁移率组蛋白B1（HMGB1）的相关性。方法采集35例烧伤体表总面积〉30％的患者静脉血样，根据是否并发多器官功能障碍综合征（MODS）分组（MODS组13例、非MODS组22例），采集患者伤后第1、3、5、7、14、21、28天的外周静脉血，采用酶联免疫吸附试验检测血浆HMGB1水平；观察外周血T淋巴细胞增殖反应和白细胞介素-2（IL-2）的产生能力，并通过流式细胞仪检测CD4^＋／CD8^＋T细胞的比值。结果严重烧伤患者伤后第1天血浆HMGB1水平即明显升高，其中伤后第1、7、21、28天MODS组HMGB1显著高于非MODS组（P〈0．05）。两组间比较，外周血T淋巴细胞增殖反应和IL-2的产生能力、CD4^＋／CD8^＋T淋巴细胞比值在伤后第1、14、21、28天MODS组显著低于非MODS组（P均〈0．05）。大面积烧伤患者伤后血浆HMGB1含量与细胞免疫功能指标包括T淋巴细胞增殖活性、IL-2含量、CD4^＋／CD8^＋T细胞比值呈显著负相关（P〈0．05）。结论大面积烧伤后T淋巴细胞免疫功能紊乱与患者并发MODS密切相关，严重烧伤患者血浆HMGB1水平的持续升高对机体细胞免疫功能异常具有显著影响。

英文摘要：

Objective To investigate the change in T cell-mediated immunity and its relationship with plasma high mobility group box-1 protein （HMGB1） levels in severely burned patients. Methods Thirty-five extensively burned patients （ 〉 30% total body surface area） were included in this study, and were divided into MODS group （n = 13） and non-MODS group （n =22）. The blood samples were collected on post burn days 1, 3, 5, 7, 14, 21 and 28. The plasma levels of HMGB1 were measured by using ELISA, and T lymphocyte proliferation response and its IL-2 production ability in peripheral blood were determined too. In addition, the ratio of CD4^＋/CD8^＋ T cells were detected by using flow cytometry. Results Plasma HMGB1 levels were markedly elevated on post burn day 1 in severely burned patients, and HMGB1 level was significantly higher in MODS group than in non-MODS group （ P 〈 0. 05 ）. Lymph proliferation response and IL-2 production of T cells in peripheral blood, and the ratio of CD4^＋/CD8^＋ T cells in MODS group were markedly lower than those in non-MODS group on post burn days 1, 14, 21 and 28 （all P 〈0. 05）. It indicated that plasma HMGB1 levels were negatively correlated to T cellular immune function parameters, including lymphocyte proliferation response, IL-2 production, and the ratio of CD4^＋/ CD8^＋ T cells in extensively burned patients （ all P 〈 0.05 ）. Conclusions Extensive burns could lead to T cellular immune dysfunction, which appears to be associated with the development of MODS. HMGB1, as an important late mediators of inflammation, might be involved in the pathogenesis of suppression of T cellmediated immunity in these patients.