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Immune cells communicate across a continuous, bidirectional circuit between the CNS and periphery. Immune cells from across the body engage CNS tissues and, in turn, are shaped by signals returning from the brain. (Left) Under peripheral equilibrium, immune effectors mobilized from visceral organs, secondary lymphoid organs, hematopoietic tissues, and the peripheral nervous system (PNS) - including CD4+ and CD8+ T cells, B cells, monocytes (top 3 cell types), NK cells, dendritic cells, mast cells, neutrophils, and innate lymphoid cells (bottom cluster of cells) - engage the CNS in a homeostatic dialogue that supports neural cell health, plasticity, and repair, sustaining a protective environment. (Right) Age-associated dysfunction across the same peripheral compartments reshapes this circuit: altered immune effectors enter the CNS and contribute to shifting the local environment toward a degenerative state in which microglia adopt disease-associated programs, astrocytes become reactive, and neurons accumulate pathology. This model underscores how the same circuitry can yield protective or pathogenic outcomes and that neurodegeneration is downstream of dysfunctional brain-immune crosstalk. Study: Neurodegeneration as a dysregulation of neuroimmune crosstalk

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Disrupted brain-immune signaling may help drive neurodegeneration

August 24, 2026

From gut-primed T cells to microglial signaling and persistent gene-regulatory states, researchers map an intricate immune network that…