Social status alters immune regulation and response to infection in macaques

• Type of Material: Article
• Authors: Noah Snyder-Mackler, Duke University; Joaquín Sanz, Université de Montréal; Jordan N. Kohn, Emory University; Jessica F. Brinkworth, Université de Montréal; Shauna Morrow, Duke University; Amanda O. Shaver, Duke University; Jean-Christophe Grenier, Universitaire Sainte-Justine Research Center; Roger Pique-Regi, Wayne State University; Zachary Johnson, Emory University; Mark Wilson, Emory University; Luis B. Barreiro, Université de Montréal; Jenny Tung, Duke University
• Language: English
• Date: 2016-11-25
• Publisher: American Association for the Advancement of Science
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2018 American Association for the Advancement of Science. All rights reserved.
• Final Published Version (URL): http://dx.doi.org/10.1126/science.aah3580
• Title of Journal or Parent Work: Science
• ISSN: 0036-8075
• Volume: 354
• Issue: 6315
• Start Page: 1041
• End Page: 1045
• Grant/Funding Information: J. S. was supported by the Fonds de recherche du Québec-Nature et technologies and the Fonds de recherche du Québec-Santé.; This work was supported by NIH grants R01-GM102562, P51-OD011132, and T32-AG000139; NSF grant SMA-1306134; the Canada Research Chairs Program 950-228993; and NSERC RGPIN/435917-2013.
• Research Categories: Anthropology, Physical; Health Sciences, Immunology

Abstract

Social status is one of the strongest predictors of human disease risk and mortality, and it also influences Darwinian fitness in social mammals more generally. To understand the biological basis of these effects, we combined genomics with a social status manipulation in female rhesus macaques to investigate how status alters immune function. We demonstrate causal but largely plastic social status effects on immune cell proportions, cell type–specific gene expression levels, and the gene expression response to immune challenge. Further, we identify specific transcription factor signaling pathways that explain these differences, including low-status–associated polarization of the Toll-like receptor 4 signaling pathway toward a proinflammatory response. Our findings provide insight into the direct biological effects of social inequality on immune function, thus improving our understanding of social gradients in health.