Numerous avenues of enquiry suggest a potential causal relationship between immune dysfunction and oxidative stress and schizophrenia. Non-resolving elevation of interleukin 6 (IL-6/IL6r) has been implicated, related to development of psychosis, present before the initiation of medication. Chronic inflammation is also a key driver of metabolic dysfunction, common in schizophrenia. Mechanistically, IL6/IL6r and related low molecular weight proteins have the ability to cross the blood-brain barrier and increase its permeability, drawing in further local inflammatory actors including nitric oxide and chemokines. Activated microglia may lead to grey matter volume (GMV) loss through excessive dendritic pruning and/or impaired surveillance and clearance of dysfunctional or pathological synapses. Thus, the immune system may be related to structural brain change via complex effects on neuronal development, micro and astrocytic function and synaptic pruning and explain increased grey matter volume loss seen in mental illness. However, whilst aberrant immune profiles may be relevant, current evidence is actually mixed, with uncertain evidence of progressive GMV loss in schizophrenia groups as a whole, PET microglial activity and relevance of peripheral measured of inflammation. A clear characterisation of a brain signature related to chronic low-level inflammation in schizophrenia, with evidence of related phenotypic profile will help advance our ability to target precision medicines. This presentation will outline recent evidence from the Psychosis Immune Mechanism Stratified Medicine Study (PIMS) focused on the phenotypic and neuro-anatomical profile of immune active psychosis from genomic, early and later stage populations using large samples and multimodal data driven approaches.