Change in T cell-mediated immunity and its relationship with high mobility group box-1 protein levels in extensively burned patients.
- Author:
Ning DONG
1
;
Bo-Quan JIN
;
Yong-Ming YAO
;
Yan YU
;
Yu-Jue CAO
;
Li-Xin HE
;
Jia-Ke CHAI
;
Zhi-Yong SHENG
Author Information
- Publication Type:Journal Article
- MeSH: Adolescent; Adult; Burns; blood; complications; immunology; Female; HMGB1 Protein; blood; Humans; Immunity, Cellular; immunology; Male; Middle Aged; Multiple Organ Failure; etiology; immunology; T-Lymphocytes; immunology
- From: Chinese Journal of Surgery 2008;46(10):759-762
- CountryChina
- Language:Chinese
-
Abstract:
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.