Alarmins link neutrophils and dendritic cells

被引:186
作者
Yang, De [1 ,2 ]
de la Rosa, Gonzalo [1 ]
Tewary, Poonam [1 ]
Oppenheim, Joost J. [1 ]
机构
[1] NCI, Mol Immunoregulat Lab, Canc & Inflammat Program, Ctr Canc Res, Frederick, MD 21702 USA
[2] SAIC Frederick Inc, Basic Sci Program, Frederick, MD 21702 USA
基金
瑞典研究理事会;
关键词
HEPARIN-BINDING PROTEIN; ANTIMICROBIAL PEPTIDE LL-37; CHEDIAK-HIGASHI-SYNDROME; NECROSIS-FACTOR-ALPHA; INFLAMMATORY MONOCYTES; SECRETORY VESICLES; SERINE PROTEASES; INNATE IMMUNITY; INDEPENDENT RELEASE; GRANULE DEFICIENCY;
D O I
10.1016/j.it.2009.07.004
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Neutrophils are the first major population of leukocyte to infiltrate infected or injured tissues and are crucial for initiating host innate defense and adaptive immunity. Although the contribution of neutrophils to innate immune defense is mediated predominantly by phagocytosis and killing of microorganisms, neutrophils also participate in the induction of adaptive immune responses. At sites of infection and/or injury, neutrophils release numerous mediators upon degranulation or death, among these are alarmins which have a characteristic dual capacity to mobilize and activate antigen-presenting cells. We describe here how alarmins released by neutrophil degranulation and/or death can link neutrophils to dendritic cells by promoting their recruitment and activation, resulting in the augmentation of innate and adaptive immune responses.
引用
收藏
页码:531 / 538
页数:8
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