The present work measured circulating antibodies against native gliadins, deamidated gliadin-derived epitopes, and transglutaminase 2 (TGM2) in 473 patients with schizophrenia and 478 control subjects among a Chinese population. The results showed that 27.1% of patients with schizophrenia were positive for the IgA antibody against native gliadins compared with 17.8% of control subjects (χ(2) = 11.52, P = .0007, OR = 1.72, 95% CI 1.25-2.35), although this significant difference appeared to be due mainly to low IgA gliadin antibody levels in female controls. A total of 27.6% of female patients were positive for IgA gliadin antibodies compared with 13.9% of female controls (χ(2) = 10.46, P = .0012, OR = 2.36, 95% CI 1.39-4.01), and 26.4% of male patients were positive for IgA antibodies compared with 19.8% of male controls (χ(2) = 3.26, P = .071, OR = 1.46, 95% CI 0.97-2.19). Of 128 patients who were positive for the IgA antibody against native gliadins, 8 were positive for the IgA antibody against deamidated gliadin epitopes and 1 was positive for IgA anti-TGM2 antibody. However, quantitative analysis demonstrated that the mean levels of IgA antibodies against deamidated gliadin epitopes and TGM2 were significantly lower in patients with schizophrenia than the control subjects (P < .001 and P = .008, respectively). The prevalence of IgG antibodies against native gliadins was not significantly different between the patient group and the control group (χ(2) = 2.25, P = .134, OR = 1.32, 95% CI 0.92-1.88). This study suggests that specific gliadin-derived epitopes may be involved in schizophrenia.