Abstract: Traumatic brain injury (TBI) is an acquired injury of the brain caused by the impact of external forces on the brain (Maas et al., 2008). It is a major cause of death and disability among people of all ages (Maas et al., 2008). The primary mechanical injury to the brain initiates a cascade of secondary biochemical events that lead to acute and chronic neurodegeneration and activation of inflammatory pathways (Maas et al., 2008). Both brain-resident microglia and blood-derived myeloid cells – macrophages and monocytes that infiltrate the brain due to injury-induced blood-brain barrier damage, contribute to the inflammatory responses after TBI (Morganti et al., 2015). These cells are responsible for clearing the damaged tissue through phagocytosis (Henry et al., 2020). This, in turn, activates the inflammasome and interferon type-1-mediated innate immune responses (Henry et al., 2020). The initial inflammatory response is important for resolving any tissue damage as it can remove the damaged cells and clear the injured area for regeneration (Henry et al., 2020). However, this is contingent on efficient degradation of phagocytosed dead cells and tissue debris by the immune cells, and their eventual transition to anti-inflammatory states to promote tissue regeneration. In TBI, neuroinflammation persists chronically and contributes to long-term pathology and poor recovery.