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Type 1 immune response reduces seizure risk after traumatic brain injury

Nature Reviews Immunology volume 25, page 234 (2025)Cite this article

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Traumatic brain injury (TBI) occurs when a sudden external force strikes the head. Days or even months after the initial impact, secondary brain injuries can increase the risk of neurological complications such as post-traumatic epilepsy. Importantly, inflammation and injury in the thalamus — a key region for cognition and sensory processing — can increase seizure risk. In this preprint (not peer-reviewed), Mroz et al. examine the progression of thalamic inflammation after TBI and the role of lymphocytes in modulating seizure risk.

To induce secondary injury in the mouse thalamus, the authors used a controlled cortical impact model of TBI. Flow cytometric analysis of micro-dissected brain regions showed delayed lymphocyte infiltration into the thalamus, peaking one month after TBI. This was distinct from cortical inflammation, which peaked around day 14. Thalamic infiltrates comprised mainly CD8+ T cells, T helper 1 cells, natural killer (NK) cells and type I innate lymphoid cells (ILC1s). Correspondingly, levels of the type 1 cytokine IFNγ were higher in the thalamus than in other brain regions after TBI.

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Original article

  • Mroz, N. M. et al. Type 1 lymphocytes and interferon-γ accumulate in the thalamus and restrict seizure susceptibility after traumatic brain injury. Preprint at bioRxiv https://doi.org/10.1101/2024.12.28.630606 (2024)

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  1. Preprint Club, University of Toronto, Toronto, Ontario, Canada

    Jennifer S. Y. Ahn & Jennifer L. Gommerman

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  1. Jennifer S. Y. Ahn
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  2. Jennifer L. Gommerman
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Correspondence to Jennifer L. Gommerman.

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Ahn, J.S.Y., Gommerman, J.L. Type 1 immune response reduces seizure risk after traumatic brain injury. Nat Rev Immunol 25, 234 (2025). https://doi.org/10.1038/s41577-025-01154-5

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  • DOI: https://doi.org/10.1038/s41577-025-01154-5

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