• Zhonghua Wai Ke Za Zhi · May 2008

    [Change in T cell-mediated immunity and its relationship with high mobility group box-1 protein levels in extensively burned patients].

    • Ning Dong, Bo-Quan Jin, Yong-Ming Yao, Yan Yu, Yu-Jue Cao, Li-Xin He, Jia-Ke Chai, and Zhi-Yong Sheng.
    • Burns Institute, First Hospital Affiliated to the Chinese Public Liberate Army General Hospital, Beijing 100037, China.
    • Zhonghua Wai Ke Za Zhi. 2008 May 15; 46 (10): 759-62.

    ObjectiveTo 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.MethodsThirty-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.ResultsPlasma 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).ConclusionsExtensive 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 cell-mediated immunity in these patients.

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