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This commentary explores the emergence of adaptive immunity in the CNS due to specific inflammatory conditions following stroke.

March 4, 2026Open Access

Organized immunity in the CNS: what stroke reveals about neuroinflammation and lymphoid niches

Puntos clave

This commentary explores the emergence of adaptive immunity in the CNS due to specific inflammatory conditions following stroke.
Analysis of experimental ischemic stroke effects on CNS immunity.
Focus on microglial MIF-CD74/CXCR4 signaling pathways.
Examination of B cell proliferation and lymphoid structures in the CNS.
Ischemic stroke led to the formation of germinal center-like B cell follicles.
Microglial signaling was crucial in inducing chronic neuroinflammation.
Observations align with the idea of ectopic lymphoid structures in various CNS conditions.

Resumen

Organized adaptive immunity can emerge in the CNS under specific inflammatory and stromal conditions. The study by Yang et al. in this issue of the JCI reports that experimental ischemic stroke induced germinal center-like B cell follicles through microglial MIF-CD74/CXCR4 signaling and in situ B cell proliferation, promoting chronic neuroinflammation. These findings align with a growing body of evidence that the brain and meninges can support ectopic lymphoid structures in multiple sclerosis, during aging, and in certain gliomas. This Commentary integrates these observations to highlight shared principles, disease-specific outcomes, and unresolved questions regarding the identity and function of lymphoid aggregates in the CNS.

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