ArticleFrontiers in psychiatry2026
Interferon-γ +874T/A polymorphism,
Article in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background and Hypothesis: Study design: We conducted a case-control study of adult males (103 cases meeting DSM-IV criteria for paranoid schizophrenia; 102 healthy controls) from two mental health centers in Israel. TG status was assessed serologically using automated ELFA/VIDAS assays. IFN-γ +874T/A was genotyped with Applied Biosystems TaqMan assays. Logistic regression modeled case status as a function of TG serostatus, genotype (AA/TA/TT), their interaction, and age. Hardy-Weinberg equilibrium (HWE) was tested among controls. Sensitivity analyses explored dominant, recessive, and additive genetic encodings. Study results: TG seropositivity rates were nearly identical in cases and controls. Genotype distributions among controls conformed to HWE. In the primary model, TG serostatus was not associated with case status, and no TG×genotype interaction was detected. Findings were consistent across sensitivity analyses. Conclusions: In this male paranoid-schizophrenia cohort, we found no evidence that TG serostatus, IFN-γ +874T/A, or their interaction contribute to disease risk. The near-identical TG+ prevalence across groups argues against large interaction effects under the exposure and measurement definitions used here. Transparent null results refine plausible effect sizes and caution against overinterpreting adult TG seropositivity as a biomarker of psychosis risk. Future studies should target developmental timing and immune-functional markers before infection-related screening or prevention can be justified.
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