期刊
BLOOD
卷 117, 期 5, 页码 1677-1686出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-06-287243
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资金
- Ministero dell'Istruzione, dell'Universita e della Ricerca [PRIN 2007H9AWXY]
- University of Verona
- Fondazione Cariverona and Associazione Italiana per la Ricerca sul Cancro [AIRC 5839]
- Associazione Italiana per la Ricerca sul Cancro
- Canadian Institutes of Health
The role of neutrophils as key players in the regulation of innate and adaptive immune responses is increasingly being recognized. We report that human neutrophils establish a network with both natural killer (NK) cells and 6-sulfo LacNAc(+) dendritic cells (slanDCs), which ultimately serves to up-regulate NK-derived interferon gamma (IFN gamma). This network involves direct reciprocal interactions and positive amplification loops mediated by cell-derived cytokines. Accordingly, we show that after lipopolysaccharide + interleukin-2 (IL-2) or IL-15/IL-18 stimulation, neutrophils directly interact with and potentiate the activity of both slanDCs and NK cells. On the one hand, neutrophils augment the release of IL-12p70 by slanDCs via a CD18/ intercellular adhesion molecule-1 (ICAM-1) interaction that stimulates activated NK cells to produce IFN gamma. IFN gamma further potentiates the interaction between neutrophils and slanDCs and the release of slanDC-derived IL-12p70, thus creating a positive feedback loop. On the other hand, neutrophils directly costimulate NK cells via CD18/ICAM-3, leading to the production of IFN gamma. Colocalization of neutrophils, NK cells, and slanDCs, as well as of IL-12p70 and IFN gamma, in inflamed tissues of Crohn disease and psoriasis provides strong evidence for a novel cellular and cytokine cooperation within the innate immune system in which neutrophils act as amplifiers of NK cell/slanDC-mediated responses. (Blood. 2011; 117(5): 1677-1686)
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