Infectious pathogens are among the strongest selective forces in mammalian evolution, allowing resistance alleles to emerge and spread over time. The host inflammatory response to such pathogens is orchestrated predominantly by cytokines, which may have evolved to shunt energy resources into fighting infectious agents and altering host behavior to avoid death from pathogen exposure1. Recently, a rich diversity of immune cells in the healthy mouse meninges have been described, where they are ideally positioned for immune surveillance of the central nervous system (CNS) and its borders2. Meningeal immune cells, and their derived cytokines, have also been shown to affect brain functions, including sociability and spatial learning3,4. Here, we sought to identify and explore additional meningeal immune populations with the potential to impact brain functions. We uncovered the molecular mechanisms by which physiological levels of interleukin-17a (IL-17a) derived from dural-associated γδ17 T cells control anxiety-like behavior in mice through neuronal IL-17Ra signaling. Our findings provide new insights into the neuroimmune interactions at the meningeal– brain interface and support further research into new therapies for neuropsychiatric conditions.
