<![CDATA[Background: Psychosis is increasingly understood as a heterogeneous neuropsychiatric syndrome in which immune dysregulation may interact with dopaminergic, glutamatergic, and neurodevelopmental mechanisms. Purpose: To synthesize evidence on neuroinflammatory pathways implicated in psychosis and evaluate their potential clinical relevance. Method: A narrative literature review was conducted through PubMed-based searching between January and June 2026. English- or Indonesian-language full-text publications issued from 2016 to 2026 were considered when they addressed psychosis or schizophrenia in relation to cytokines, chemokines, immune-cell profiles, microglial activation, blood–brain barrier dysfunction, oxidative stress, or the gut–brain axis. Ten highly relevant review-level articles were selected and narratively synthesized using a PICOS-informed extraction framework. Results: Across the included literature, psychosis was associated with increased pro-inflammatory mediators, particularly interleukin-6, interleukin-1β, tumor necrosis factor-α, interferon-γ, C-reactive protein, and selected chemokines. Peripheral immune-cell alterations, microglial activation, oxidative stress, impaired blood–brain barrier integrity, and microbiome-related immune signaling were repeatedly reported. These processes may disrupt synaptic pruning, N-methyl-D-aspartate receptor signaling, inhibitory interneuron function, and dopamine–glutamate balance. However, heterogeneity across disease stage, medication exposure, comorbidity, biospecimen, and assay method limits diagnostic specificity. Conclusion: Neuroinflammation is a plausible contributor to the pathophysiology and progression of psychosis, but current biomarkers are better viewed as stratification or prognostic candidates than stand-alone diagnostic tests. Longitudinal, multimodal, and phenotype-stratified studies are required before immune-targeted interventions can be incorporated into routine care.]]>
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