It is widely accepted that the crosstalk between the nervous and immune system is bidirectional, highly regulated, and crucial for survival. In the brain, microglia intermediate this relationship, assist in remodeling neuronal circuits, and respond to cytokines produced by infection (Th1 axis) or allergic reactions (Th2 axis). In the womb, the maternal environment is biased towards Th2 to support both the fetus and its neurodevelopment. Yet, as certain brain regions switch from exuberant growth to circuit pruning, we propose that a move away from Th2 is not only physiological but desired.
Recently, we discovered that cerebellar remodeling in the early postnatal period is driven by microglia engulfing of neuronal material. We also found that prematurely rising the levels of Th2 cytokines leads to aberrant cerebellar maturation and lasting circuit alterations. Additionally, we show that allergic challenges during the early postnatal period are sufficient to drive an hyperkinetic and impulsive-like phenotype in mice, reminiscent of Attention-Deficit/Hyperactivity Disorder (ADHD). Together, our findings demonstrate a critical role for Th2 cytokines in postnatal neurodevelopment and provide mechanistic insight into the reported overlap between allergies and hyperkinetic disorders such as ADHD and Tourette syndrome.