The social status of a rhesus macaque affects the nature of its immune system, where low-status animals show greater antibacterial responses and high-status animals tend to have greater antiviral responses. The results could hint at important parallel effects in humans, where social status is known to drive health inequalities. Differences in resources and health risk behaviors have been shown to drive health inequalities in humans. Yet, studies in animal species with social constructs similar to humans suggest that these inequalities may also have a biological basis. To test how social status influences immune system function at the molecular and cellular level, Noah Snyder-Mackler et al. manipulated the social ranks of 45 female macaques in captivity, introducing new members to a group once a hierarchy was already established. "High-ranking" females were found to have greater levels of certain types of T cells, and, in particular, greater levels of natural killer cells, which respond quickly to viral infections, compared to females of lower social status. Stress that results from social subordination was identified as important in shaping immune-related gene expression in low-status individuals, though when the researchers adjusted for the fact that lower social status also means less grooming, they found that this lack of positive social interactions may be equally or even more important. Next, in petri dishes, the team simulated bacterial infection in blood samples from the monkeys, analyzing the immune response. They found that the immune responses of lower status females demonstrated significantly greater production of proinflammatory cytokines, which respond to bacterial infection. Thus it appears that, in macaques, social subordination promotes antibacterial responses, while high social status promotes anti-viral responses. In a related Perspective, Robert M. Sapolsky discusses how these findings relate to socioeconomic status and health inequalities in humans.