Abstract: Traumatic brain injury (TBI) is a significant public health issue, affecting approximately 1.7 million people annually in the United States alone, with over 5 million experiencing long-term disabilities (Roozenbeek et al., 2013). A major sequela of TBI is long-lasting white matter injury (WMI) which includes traumatic axonal injury and loss of myelination, resulting in cognitive, behavioral, and psychiatric deficits in survivors. To date, there are no effective therapies for traumatic WMI, and novel therapeutic approaches are urgently needed. Oligodendrocytes, which provide metabolic support to axons and are the producers of myelin in the central nervous system (CNS), undergo apoptosis after TBI, triggered by direct injury or in response to axonal degeneration (Flygt et al., 2016, 2017). Mature oligodendrocytes present in the brain at the time of injury have limited, if any, capability to contribute to remyelination. Therefore, the bulk of CNS remyelination is attributed to the differentiation of oligodendrocyte progenitor cells (Franklin and Ffrench-Constant, 2017), which can be adversely impacted by inflammation after TBI. This highlights that initial WMI from TBI is amplified by a failure of post-injury reparative mechanisms. Understanding the molecular and cellular mechanisms by which inflammation impairs oligodendrocyte progenitor cell proliferation and remyelination is thus essential to identify targetable post-injury processes to improve recovery.