Journal
CELL REPORTS
Volume 29, Issue 5, Pages 1178-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.09.046
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Funding
- NHMRC of Australia [APP1045755, APP1126636, APP1044152]
- Monash University, Faculty of Medicine, Nursing, and Health Sciences
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Traumatic brain injury (TBI) leaves many survivors with long-term disabilities. A prolonged immune response in the brain may cause neurodegeneration, resulting in chronic neurological disturbances. In this study, using a TBI mouse model, we correlate changes in the local immune response with neurodegeneration/neurological dysfunction over an 8-month period. Flow cytometric analysis reveals a protracted increase in effector/memory CD8(+) T cells (expressing granzyme B) in the injured brain. This precedes interleukin-17(+)CD4(+) T cell infiltration and is associated with progressive neurological/motor impairment, increased circulating brain-specific autoantibodies, and myelin-related pathology. Genetic deficiency or pharmacological depletion of CD8(+) T cells, but not depletion of CD4(+) T cells, improves neurological outcomes and produces a neuroprotective Th2/Th17 immunological shift, indicating a persistent detrimental role for cytotoxic T cells post-TBI. B cell deficiency results in severe neurological dysfunction and a heightened immune reaction. Targeting these adaptive immune cells offers a promising approach to improve recovery following TBI.
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