Enter the encephalitis_verse: a translational programme decoding how viral and autoimmune attacks reshape neuronal circuits, synapses and long-term neurological outcome.
Encephalitis can be triggered by viral infection, post-infectious autoimmunity or primary autoimmune responses. Even when the acute inflammation resolves, many patients are left with seizures, cognitive impairment, behavioural symptoms and long-term neurological disability.
Our central question is how protective immune responses become damaging: how T cells, antibodies and CNS phagocytes reshape neuronal circuits, strip synapses and make neurons vulnerable to degeneration.
The encephalitis_verse combines rare human brain tissue, single-nucleus and spatial transcriptomics, multiplex imaging, CSF proteomics and causal in vivo models to identify mechanisms, biomarkers and therapeutic opportunities.
From immune activation to synaptic dysfunction. Multiplex immunofluorescence, whole-slide imaging and high-resolution confocal microscopy reveal how inflammatory niches emerge within the brain and how they drive complement deposition, phagocyte activation and synaptic elimination.
Representative multimodal microscopy and 3D reconstructions from the encephalitis_verse programme.
How do CD8⁺ T cells, antibodies and CNS phagocytes disrupt synaptic connectivity before irreversible neuronal loss occurs?
Which cellular neighborhoods sustain chronic inflammation inside human brain tissue, and how do they relate to infected cells, glia and vulnerable neurons?
Do viral, post-infectious and autoimmune encephalitis converge onto common pathways of synaptic dysfunction and neurodegeneration?
Can molecular signatures in tissue and CSF predict outcome and reveal pathways that can be targeted without compromising antiviral immunity?
Immune activation can resolve, but in many patients it leaves persistent neurological sequelae through synaptic dysfunction and neuronal damage.
Neuronal STAT1–CCL2 signalling recruits phagocytes and drives synaptic loss during CD8⁺ T-cell attack.
Human Neuro-HIV tissue reveals GPNMB/LGALS3/CTSB phagocyte states associated with synapse engulfment.
Intracellular-antigen AE shows neuronal pSTAT1, resident memory CD8⁺ cells and GPNMB⁺ phagocytes.
IgLON5 disease is framed as an autoantibody-first cascade leading to secondary tauopathy.
A unifying model where neuronal STAT1 shifts from antiviral defense to durable synaptopathy when sustained.
From fundamental mechanisms to translational neuroimmunology.
First demonstration that neurons under CD8⁺ T-cell attack engage a STAT1–CCL2 programme that recruits phagocytes, drives synaptic stripping and produces neurological disease.
Read article →
Post-mortem human brain tissue revealed LGALS3⁺/GPNMB⁺/CTSB⁺/HLA-DR⁺ CNS phagocytes topographically linked to inflammation and synaptic stripping.
Read article →
Across a multicentre human cohort, intracellular-antigen AE was defined by neuronal pSTAT1, brain-resident memory CD8⁺ T cells and GPNMB⁺ phagocytes with synaptic engulfment.
Read article →
A conceptual framework for IgLON5 disease in which antibody binding initiates nuclear stress and a downstream tauopathy — highlighting the importance of early treatment windows.
Read article →
A unifying model proposing that neuronal pSTAT1 is protective during acute antiviral responses but becomes maladaptive when interferon signalling persists.
Read article →A compact record of awards, publications and milestones shaping the transition from neuroinflammation to neurodegeneration research.
Support for a translational programme investigating immune-mediated synaptopathy and neuronal injury in encephalitis.
A conceptual framework proposing neuronal STAT1 as a phase switch from antiviral defence to synaptopathy.
Neuronal pSTAT1, resident memory CD8⁺ T cells and GPNMB⁺ phagocytes define T-cell-mediated autoimmune encephalitis.
Understanding how immune responses reshape the brain today may reveal how to prevent permanent neurological injury tomorrow.
Department of Basic Neuroscience, University of Geneva · Clinical and translational links with CHUV and collaborating neuropathology centres.
Giovanni Di Liberto investigates how immune responses reshape neuronal circuits during viral and autoimmune encephalitis. His work bridges clinical neurology, human neuropathology and experimental neuroimmunology to understand how neuroinflammation becomes neurodegeneration.