Immunological Evidence between Schizophrenia and Toxoplasmosis : an Overview

Results: Studies have shown that patients with schizophrenia have significantly increased levels of antibodies to T. gondii compared with healthy controls. Previous research has shown an increase in the antibody response to Toxoplasma proteins in schizophrenia and bipolar disorders. CD8 immunity is reduced in schizophrenic patients, it is conceivable that a partial loss of CD8 functionality could result in periodic reactivation of the quiescent T. gondii parasites, resulting in focal necrosis and localized inflammation (contributed by innate immune cell-produced cytokines).

etiology of Schizophrenia, and it is now considered a possible cause of this pathology.Transient symptoms of acute toxoplasmosis sometimes resemble the clinical picture of paranoid schizophrenia and studies have shown that patients with schizophrenia have significantly increased levels of antibodies to T. gondii compared with healthy controls.

Results
Previous research has shown an increase in the antibody response to Toxoplasma proteins in schizophrenia and bipolar disorders [1].A study performed on US soldiers found that the first occurrence of anti-Toxoplasma antibodies was detected in frozen blood samples collected from subjects that were later demilitarized because of their psychiatric disease 6 months and often even 2-3 years before the onset of the schizophrenia [2].Experimental study demonstrated that Psychiatric patients have increased rates of toxoplasma antibodies, the differences between cases and controls being greatest in individuals who were assayed near the time of the onset of their symptoms [3].Of the 192 individuals examined, patients with schizophrenia had significantly increased levels of serum IgG antibodies to T. gondii (57.1%) as compared to controls (29.2%)(p < 0.05).The OR for this association was 2.99 with 95% CI = 1.65−5.41[4].
Emelia et al. [5] found, after an analysis of 288 serum samples from schizophrenic patients (n=144) and psychiatrically healthy volunteers (n=144), a significant result in the sero intensity rate of anti-T.gondii IgG antibody (> 60 IU/mL) in schizophrenic patients (61.1%) as compared to psychiatrically healthy volunteers (40.8%) (X² = 4.236, p < 0.050).Pedersen et al. [6] found a significant positive association between T. gondii IgG antibody level and schizophrenia spectrum disorders.For the authors the mothers with the highest IgG level had a relative risk of 1.73 (95% confidence interval [CI]=1.12-2.62)compared with mothers with the lowest IgG level.
Studies of schizophrenic patients have revealed dampened CD8 T-cell immunity in such subjects [7].Memory CD8 T cells are believed to persist life long, and reencounter with the pathogen can mediate protective responses in self-resolving infectious diseases.However, recent laboratory studies have reported progressive loss of CD8 T cell functionality (dysfunction in terms of proliferation, cytotoxicity, cytokine production, and survival) during chronic toxoplasmosis in certain strains of mice [8].For Bhadra et al. [9] as CD8 immunity is reduced in schizophrenic patients, it is conceivable that a partial loss of CD8 functionality could result in periodic reactivation of the quiescent T. gondii parasites, resulting in focal necrosis and localized inflammation (contributed by innate immune cellproduced cytokines).Such accrued damage of nervous system potentially over time could result in some of the various forms of mental impairment [9].
Besides, T. gondii can invade and multiply inside any nucleated cell type including epithelial cells and blood leukocytes.Studies in mice indicate that the dendritic cells as well as monocytes/macrophages function as systemic parasite transporters ("Trojan horses") during infection [10].

Conclusions
Therefore, although there were varied theoretical models that aim to explain the pathogenic mechanism of Toxoplasma infection in the brain, your correlation with Schizophrenia it´s difficult to establish.It will be necessary more experimental researches and clinical trials giving emphasis on these correlations.Then design effective public policies and protocols tracking for Schizophrenia it might be a possible reality.