Autoimmunity and Traumatic Brain Injury

Purpose of Review Traumatic brain injury (TBI) causes injured brain cells to release brain-specific proteins, which may trigger an autoantibody response. In this review, we will discuss how autoimmunity is triggered after TBI and summarize the identified brain antigens to which an autoimmune response has been observed as well as their clinical implications. Recent Findings TBI leads injured brain cells to release brain proteins, in their intact or proteolytic fragment form, into extracellular fluids and eventually into circulating blood. These brain proteins treated by the immune system as foreign antigens can evoke the systemic production of both IgM and IgG isoforms. Increasing evidence shows that in a subset of TBI patients, there are circulating autoantibodies recognizing a range of brain proteins, including glial proteins like S100B, glial fibrillary acidic protein, and peroxirerdoxin; neuroreceptors such as glutamate receipt subunits NR1; and oligodendrocyte-originated myelin basic protein. Summary Autoimmunity is triggered in TBI, targeting a range of brain-specific antigens in a subset of TBI patients. Such autoantibodies might be useful for biofluid-based diagnosis in order to identify patients who might benefit from immunotherapy.