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.