Elevated proinflammatory cytokines are found in the brain and the blood from schizophrenia cases and are used to define the “high” and “low” inflammatory biotypes. Cytokines elevated in schizophrenia mediate IgG release and effector functions. Yet, whether IgG, its transporter (FcGRT), proinflammatory receptors (like FcGR3A) and anti-inflammatory receptor (FcGR2B) contribute to schizophrenia neuropathology is unknown. B cells which produce IgG predominantly reside in the periphery thus brain-reactive IgG is likely found in the blood. Thus, I investigated brain-reactive IgG presence and abundance in the blood from people with schizophrenia and healthy controls. I found IgG surrounding blood vessels in the prefrontal cortex (PFC) and midbrain, but IgG only localised to cells in the midbrain from some schizophrenia cases and control subjects indicating that IgG interactions differ between brain regions. IgG and FcGRT protein abundance are unchanged in the PFC and midbrain when comparing the two diagnostic groups irrespective of inflammatory biotype. FcGRT mRNA was unchanged in the PFC. FcGRT and FcGR3A mRNA levels were elevated in the midbrain from “high inflammation” biotype schizophrenia cases while FcGR2B mRNA was unchanged, suggesting an imbalance between Fcγ receptor mediated pro- to anti- inflammatory signalling. Principal axis factoring revealed that mRNA levels of FcGR3A and phagocytic cell markers (AIF, CD68, CD163, HLA-DR) formed one factor in the midbrain from “high inflammation” biotype schizophrenia cases. While mRNA levels of FcGR2B, FcGRT, and BBB markers [astrocytes (GFAP) and activated endothelial cells (ICAM)] formed another factor. Thus, FcGR3A-mediated phagocytosis may contribute to midbrain pathology in schizophrenia. I found IgG in the blood from people with schizophrenia and healthy controls targets monkey cerebellum structures. Brain-reactive IgG abundance is decreased in plasma from people with schizophrenia. Decreased brain reactive IgG correlated with longer illness duration of “high inflammation” biotype people with schizophrenia and increased symptom severity of “low inflammation” biotype people with schizophrenia, suggesting that insufficient brain-reactive IgG may contribute to schizophrenia neuropathology. Overall these results indicate that brain-resident IgG and brain-targeting IgG in the blood are normal occurrences. Instead, changes in how cells in the brain and IgG interact may contribute to schizophrenia neuropathology.