Th17 effector cytokines induce shared and distinct microglial and endothelial cell responses in post-streptococcal encephalitis.

ABSTRACT: Group A Streptococcus (GAS) infections can lead to neuropsychiatric sequelae in children, yet the mechanisms driving post-infectious brain pathology remain poorly defined. In a mouse disease model, Th17 lymphocytes induce microglial activation, blood-brain barrier (BBB) dysfunction, and neural circuit impairment; however, the transcriptional programs underlying these effects, and the specific Th17-derived cytokines involved are unclear. Using mouse genetics, single-cell RNA sequencing, and spatial transcriptomics, we show that GAS infections induce inflammatory gene programs in microglia and brain endothelial cells (BECs), accompanied by downregulation of BBB-associated transcripts in BECs. Spatial transcriptomic analyses reveal that GAS-responsive microglia are enriched near infilt

SUBMITTER: Wayne CR 

PROVIDER: S-EPMC12889615 | biostudies-literature | 2026 Feb

REPOSITORIES: biostudies-literature