Traumatic brain injury (TBI) is an ever growing health concern, with cases increasing in both the US and the world at large. With the improvement of emergency medicine in recent decades, survival from TBI has become more common place, and thus individuals are coping with long-term deleterious outcomes from trauma as a result. Such outcomes include altered cognitive (memory loss/executive function), social (isolation tendencies), and behavioral (risk-taking behavior/anxiety) function. Researchers use preclinical rodent models to investigate cellular and molecular underpinnings of adverse TBI outcomes. One leading mechanism of long-term cognitive changes include alterations of immune function in the brain (termed 'neuroimmune'). Studies have found that TBI can induce chronic maladaptive neuroimmune responses, which can in turn propagate long-term neurological deficits. Unfortunately, most of the molecular understanding of TBI-induced neuroimmune outcomes is derived from studies performed solely in males. This is especially problematic as sex-dimorphic neuroimmune changes have been identified in healthy individuals. If and how these basal neuroimmune differences influence TBI related outcomes is the focus of this short review. Importantly, understanding these differences could allow for improved therapeutic development for treating the long-term effects of TBI.