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Depressive symptoms and immune transcriptional profiles in late adolescents
•Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes,...
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Published in: | Brain, behavior, and immunity behavior, and immunity, 2019-08, Vol.80, p.163-169 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | •Depressed mood was linked to upregulated expression inflammation-related genes.•Depressed mood was linked to downregulated expression of antiviral-related genes.•This pattern was mediated by greater NF-κB activity and reduced GR and IRF activity.•Cellular sources of this pattern included monocytes, B cells, and dendritic cells.
Rates of depression increase and peak during late adolescence and alterations in immune processes are thought to be both a risk factor and outcome of depression. However, few studies have examined depression-immune dynamics among adolescents. Using a functional genomics approach, the current study examined whether depressive symptoms were associated with activation of a gene expression profile, characterized by upregulated expression of pro-inflammatory-related genes and downregulated expression of antiviral-related genes in a sample of older adolescents (Mage = 18.37, SD = 0.51).
Participants (n = 87) reported on their depressive symptoms during the past week using the CES-D, and provided blood samples for genome-wide transcriptional profiling of mRNA.
Adolescents with clinically-significant levels of depressive symptoms (CES-D ≥ 16) exhibited upregulated expression of inflammation-related genes and downregulated expression of antiviral-related genes compared to their peers with lower levels of depressive symptoms (CES-D |
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ISSN: | 0889-1591 1090-2139 |
DOI: | 10.1016/j.bbi.2019.03.004 |