Journal
JOURNAL OF INNATE IMMUNITY
Volume 9, Issue 1, Pages 94-108Publisher
KARGER
DOI: 10.1159/000450576
Keywords
Mast cells; Natural killer cells; Innate immunity; Viral infection; Interferons; Cytokines; Allergy
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Funding
- Consejo Nacional de Ciencia y Tecnologia (CONACYT), Mexico [147763, 181205]
- Canadian Institutes of Health Research (CIHR) [MOP-10966]
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Mucosal surfaces are protected from infection by both structural and sentinel cells, such as mast cells. The mast cell's role in antiviral responses is poorly understood; however, they selectively recruit natural killer (NK) cells following infection. Here, the ability of virus-infected mast cells to enhance NK cell functions was examined. Cord blood-derived human mast cells infected with reovirus (Reo-CBMC) and subsequent mast cell products were used for the stimulation of human NK cells. NK cells upregulated the CD69 molecule and cytotoxicity-related genes, and demonstrated increased cytotoxic activity in response to Reo-CBMC soluble products. NK cell interferon (IFN)-gamma production was also promoted in the presence of interleukin (IL)-18. In vivo, SCID mice injected with Reo-CBMC in a subcutaneous Matrigel model, could recruit and activate murine NK cells, a property not shared by normal human fibroblasts. Soluble products of Reo-CBMC included IL-10, TNF, type I and type III IFNs. Blockade of the type I IFN receptor abrogated NK cell activation. Furthermore, reovirus-infected mast cells expressed multiple IFN-alpha subtypes not observed in reovirus-infected fibroblasts or epithelial cells. Our data define an important mast cell IFN response, not shared by structural cells, and a subsequent novel mast cell-NK cell immune axis in human antiviral host defense. (C) 2016 S. Karger AG, Basel
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