Complement components including C5a, C3, and C1q also have well-characterized dual roles in maternal response to infection and neurodevelopment (i.e., synaptic pruning), and dysregulation of complement has been implicated in maternal infection-associated neurocognitive deficits in offspring (Stevens et al., 2007; Schafer et al., 2012; McDonald et al., 2015a; Weckman et al., 2018). Here, C5AR1 is linked to infection.