Trauma equals danger-damage control by the immune system

被引：127

作者：

Stoecklein, Veit M. ^{[1
]}

Osuka, Akinori ^{[1
]}

Lederer, James A. ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Surg, Boston, MA 02115 USA

来源：

JOURNAL OF LEUKOCYTE BIOLOGY | 2012年 / 92卷 / 03期

基金：

美国国家卫生研究院;

关键词：

injury; inflammation; macrophages; T regulatory cells (Tregs); alarmins; DAMPs; REGULATORY T-CELLS; TUMOR-NECROSIS-FACTOR; TYROSINE KINASE-3 LIGAND; COLONY-STIMULATING FACTOR; HEMORRHAGIC-SHOCK; SUPPRESSOR-CELLS; THERMAL-INJURY; INTERLEUKIN-12; PRODUCTION; SEPTIC SHOCK; RECEPTOR;

D O I：

10.1189/jlb.0212072

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Traumatic injuries induce a complex host response that disrupts immune system homeostasis and predisposes patients to opportunistic infections and inflammatory complications. The response to injuries varies considerably by type and severity, as well as by individual variables, such as age, sex, and genetics. These variables make studying the impact of trauma on the immune system challenging. Nevertheless, advances have been made in understanding how injuries influence immune system function as well as the immune cells and pathways involved in regulating the response to injuries. This review provides an overview of current knowledge about how traumatic injuries affect immune system phenotype and function. We discuss the current ideas that traumatic injuries induce a unique type of a response that may be triggered by a combination of endogenous danger signals, including alarmins, DAMPs, self-antigens, and cytokines. Additionally, we review and propose strategies for redirecting injury responses to help restore immune system homeostasis. J. Leukoc. Biol. 92: 539-551; 2012.

引用

页码：539 / 551

页数：13

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