The role of autoimmunity after traumatic brain injury

Abstract Traumatic brain injury (TBI) is a leading cause of death and disability in the United States and around the world. The primary injury (acute phase) to the brain destroys or damages the neuronal and glial cells and compromises the tissue and blood–brain barrier (BBB) integrity. The secondary injury is a prolonged phase causing cellular, molecular, and functional deficits. TBI evokes systemic and local inflammatory responses. Immune cells migrate to the brain and gain access to the brain parenchyma due to BBB breakdown. The damaged or destroyed cells, displaced proteins or their metabolites are recognized by the immune cells as autoantigens. The autoantibodies generated may be useful as biomarkers of disease severity. The autoimmunity thus developed has a long-lasting effect on the body and can be directed to the brain causing neurodegenerative disorders or elicit systemic autoimmune disorders. Hypopituitarism is one of the major pathophysiological consequences of TBI autoimmunity.