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Immune system influenced by social status, but access to resources not to blame

November 28, 2016

Social status is one of the most important factors in predicting the risk of disease and mortality in humans and other social mammals. A new study by the University of Montreal, Duke University (USA), and Emory University (USA) published in Science reveals that low social status alone can alter immune regulation, even in the absence of variation in access to resources, health care, and at-risk behaviours for health.

"In short, two individuals with access to the same dietary resources and the same health care and exhibiting the same behaviours have different immune responses to infection depending on whether they have a high or low social status," said Luis Barreiro, Professor in the Department of pediatrics at the University of Montreal's Faculty of Medicine and researcher at the Sainte-Justine University Hospital Research Center.

Macaques, close relatives of humans

To demonstrate the biological basis of the influence of social status on the immune system, the researchers combined genomics with manipulation of the social status of 45 female macaques, a species close to humans and having a linear and stable social hierarchy.

"We used macaques because it is impossible to conduct this experiment on humans for obvious ethical reasons," explained Professor Barreiro, who co-led the study with Professor Jenny Tung. "For the moment, we have only used females, but we hope to reproduce the study with males in the near future."

The researchers formed nine groups of females who lived together for one year. They then formed new groups to upset the dominance ranks among the females and study the effect of the changes on their immune systems. The researchers ensured that all the animals had access to as much food as needed, and veterinarians regularly checked that they were not sick or injured, to control for these variables.

Inflammatory vs. antiviral immune responses

In analyzing the results, the researchers discovered that the cells of macaques with low social status had a stronger pro-inflammatory response to infection compared to the cells of individuals with high social status. A pro-inflammatory response occurs when the immune system causes inflammation (e.g., redness, heat, swelling) to neutralize and eliminate bacterial or viral infections. Strong tissue or organ inflammation can save the life of the infected individual; however, disproportionate inflammation can damage the organs and leave after-affects. This may partly explain why people with low social status have a higher risk of developing cardiovascular and inflammatory diseases. For their part, macaques with high social status showed a stronger antiviral immune response compared to those with low social status.

Reversible immune differences

In addition, the researchers observed that these differences in immune responses were reversible. Indeed, when a low social status macaque achieved high social status, its immune system adopted the immune response associated with high social status.

What to do with the results?

Should this discovery encourage our societies to level out differences in social status as much as possible? Professor Barreiro does not believe so: "The history of mankind has shown us that there will always be inequalities in human society. In my opinion, the thing to do is to understand as best as possible how our immune system works and what fringes of the population are more at risk of suffering from a certain disease, and to find solutions in this regard," he concluded.
-end-
About the study

N. Snyder-Mackler, J. Sanz, J. N. Kohn, J. F. Brinkworth, S. Morrow, A.O. Shaver, J.-C. Grenier, R. Pique-Regi, Z. P. Johnson, M. E. Wilson, L. B. Barreiro, and J. Tung, "Social status alters immune regulation and response to infection in macaques", Science, November 25, 2016.

Funding for the study

The study was supported by grants from the National Institutes of Health (USA), the National Science Foundation (USA), the Canada Research Chairs Program, the Natural Sciences and Engineering Research Council of Canada, and the Fonds de recherche du Québec.

University of Montreal

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