Please use this identifier to cite or link to this item: http://hdl.handle.net/10419/67180
Authors: 
Cole, Steven W.
Conti, Gabriella
Arevalo, Jesusa M.
Ruggiero, Angela M.
Heckman, James J.
Suomi, Stephen J.
Year of Publication: 
2012
Series/Report no.: 
Discussion Paper Series, Forschungsinstitut zur Zukunft der Arbeit 6915
Abstract: 
To identify molecular mechanisms by which early life social conditions might influence adult risk of disease in rhesus macaques (Macaca mulatta), we analyze changes in basal leukocyte gene expression profiles in 4-month-old animals reared under adverse social conditions. Compared to the basal condition of maternal rearing (MR), leukocytes from peer-reared (PR) animals and PR animals provided with an inanimate surrogate mother (surrogate/peer reared; SPR) show enhanced expression of genes involved in inflammation, cytokine signaling, and T lymphocyte activation, and suppression of genes involved in several innate antimicrobial defenses including Type I Interferon antiviral responses. Promoter-based bioinformatic analyses implicate increased activity of CREB and NF-kB transcription factors and decreased activity of Interferon Response Factors (IRFs) in structuring the observed differences in gene expression. Transcript origin analyses identify monocytes and CD4+ T lymphocytes as primary cellular mediators of transcriptional up-regulation and B lymphocytes as major sources of down-regulated genes. These findings show that adverse social conditions can become embedded within the basal transcriptome of primate immune cells within the first 4 months of life, and they implicate sympathetic nervous system-linked transcription control pathways as candidate mediators of those effects and potential targets for health-protective intervention.
Subjects: 
immune system
gene expression
stress
social adversity
development
primates
JEL: 
I12
J13
Document Type: 
Working Paper

Files in This Item:
File
Size
610.13 kB





Items in EconStor are protected by copyright, with all rights reserved, unless otherwise indicated.