Abstract
The etiopathogenesis of schizophrenia is complex and involves the interaction between genetic and environmental factors. Changes in the immune system have been identified as possible participants in the pathophysiology of schizophrenia. In this paper, we present a narrative review on immune changes in the pathophysiology of schizophrenia and the potential ofmolecules and/or mechanisms of the immune system to work as biomarkers and/or therapeutic targets. While some studies show greater participation of cytokines such as T helper cells (Th1), interferon gamma (IFN-γ), interleukin 2 (IL-2), and tumor necrosis factor alpha (TNF-α), others have observed increased participation of the Th2-type cytokines IL-4, IL-6, and IL-10. Infection by the protozoan Toxoplasma gondii has been identified as a risk factor for schizophrenia, and a possible explanation could be the shift in the balance of tryptophan metabolism, with consequent increase in kynurenines caused by the inflammatory response against the parasite. Clinical trials have been conducted using anti-inflammatory drugs as adjunct strategies to antipsychotic treatment. Promising results, such as reduced negative symptoms and cognitive improvement,have been observed. The use of anti-inflammatory drugs with consequent clinical improvement reinforces the hypothesis of the participation of immune/inflammatory mechanisms in the pathophysiology of schizophrenia.
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