UCLA

Previous research has shown that adverse social conditions may promote a conserved transcriptional response to adversity (CTRA) involving up-regulation of proinflammatory gene expression and down-regulation of Type I interferon anti-viral genes in circulating blood cells. However, the impact of social conditions on lymphoid tissue gene regulation remains largely unexplored. This project assessed how social instability in adult male rhesus macaques (N=10, 5 in unstable, and 5 in stable social conditions) might regulate gene expression within secondary lymphoid tissue (lymph nodes; LN). Unstable social conditions down-regulated axillary LN expression of genes involved in Type I interferon anti-viral responses. Transcript origin analyses implicated monocytes and B cells as cellular mediators of these effects, and promoter-based bioinformatics analyses indicated reduced activity of AP-1, NF-κB, IRF, and CREB transcription factors within the axillary LN microenvironment. Although the current study is limited in sample size, these results suggest that social influences on immune cell gene regulation extend beyond the circulating leukocyte pool to alter generalized transcriptome profiles in secondary lymphoid tissue, and they do so in a regulatory program that resembles the pattern of antiviral inhibition previously observed in circulating leukocytes.