CD8A and encephalitis: This was supported by the clustering of these features (Fig. 5i) with IC-AE and other severe forms of encephalitis, such as fulminant AMPAR-antibody encephalitis (AMPAR*), which also showed high levels of neuronal pSTAT1 expression (Fig. S1e), thus suggesting a shared pathway involving CD8 + TRM cells in the pathogenesis of these debilitating neurological conditions.