Experimental study reveals gut infections establish long-lived memory CD4+ T cells in the meninges, highlighting a direct immune bridge protecting central nervous system borders.
Key Points
Investigate whether gastrointestinal infections establish long-term, pathogen-specific CD4+ T cell immunological memory within the meningeal borders of the central nervous system.
Challenged animal models with intracellular bacteria, extracellular bacteria, or parasites via the gastrointestinal tract.
Tracked the trafficking and polarization of gut-activated CD4+ T cells to the dura mater, dural venous sinuses, and brain tissue.
Evaluated the role of the CXCR6–CXCL16 chemokine axis in central nervous system homing and measured memory recall responses following systemic rechallenge.
Intestinal infections reprogrammed dural CD4+ T cell profiles into distinct TH1, TH17, or TH2 polarization states mirroring the specific enteric pathogen.
Gut-primed CD4+ T cells localized to dural lymphoid aggregates and venous sinuses via CXCR6–CXCL16 signaling to form permanent resident memory pools.
Dural memory cells demonstrated rapid recall capacity upon intravenous antigen re-exposure, proliferating extensively and secreting effector cytokines.