Type 1 lymphocytes accumulate in the thalamus and produce interferon-gamma to restrict seizure susceptibility after brain injury

We determiend that TBI elicits the emergence of dissease-associated microglial (DAM) and type 1 interferon-responsive microglial (IRM) transcriptional states within thalamic microglia (as compared to sham controls), and that the DAMs display evidence of an interferon gamma (IFNg)-driven gene signature.

We further determine that adminitration of anti-CD4 depleting antibodies increases the abundance of DAM and IRM clusters and enhances the IFNg-signature within DAMs (as compared to isotype-treated, injured controls), demonstrating enhanced interferon responses with CD4+ T cell depletion.