Journal
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
Volume 35, Issue 7, Pages 554-562Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/jir.2014.0052
Keywords
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Funding
- National Institutes of Health U01 grant [AI083005-01]
- Georgia Research Alliance
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Influenza infection causes an increase in indoleamine 2, 3-dioxygenase (IDO) activity in the lung parenchyma. IDO catabolizes tryptophan into kynurenine, leading to immune dampening. Multiple cell types express IDO, and while IFN- upregulates IDO in dendritic cells and macrophages, it is unclear how IDO is affected in respiratory epithelial cells during influenza infection. In this study, the role of IFN- in IDO regulation was investigated after influenza infection of respiratory epithelial cells. IDO1 expression increased concurrently with IFN- expression. In differentiated NHBE cells, the IDO metabolite was released basolaterally. Recombinant IFN- upregulated IDO1 activity, and silencing of IFN- decreased IDO1 expression during influenza infection. During IFN- stimulation, most differentiated cell types are able to express IDO but during influenza infection, IDO is primarily expressed in uninfected cells. These studies show a role for IDO in the host response to influenza infection, and they provide insights into novel approaches for enhancing vaccine responses and therapeutic approaches.
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