Letter to the EditorGliadin-related antibodies in schizophrenia
Section snippets
Funding source
This work was supported by NIMH R34 MH100776-01 (Eaton and Kelly).
Contributors
DLK and WWE were the principal investigators for the project, designed the protocol and oversaw the study. They participated in the manuscript writing and final draft. DC directed all the laboratory analyses and wrote the first draft of the manuscript. HKD and KR assisted in the study coordinator and data collection and contributed to the manuscript writing. MVT run all the laboratory assays. UHH assisted DC in analyses of the data and manuscript writing. SF helped to implement the study,
Disclosures
All authors declare that they have no conflicts of interest.
Acknowledgements
The authors would like to thank Martin Cihak for his regression analysis.
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Cited by (13)
The relationship of peripheral inflammation with antibodies to gliadin (AGA IgG) in persons with schizophrenia
2023, Schizophrenia ResearchImmunologic profiling in schizophrenia and rheumatoid arthritis
2022, Psychiatry ResearchElevated anti-gliadin IgG antibodies are related to treatment resistance in schizophrenia
2019, Comprehensive PsychiatryCitation Excerpt :Although the pathogenesis of schizophrenia is unclear, several studies suggest that it is associated with immunologic factors [3–6]. Recent studies report that approximately 20–30% patients with schizophrenia are positive for anti-gliadin IgG (AGA-IgG) compared to <10% in controls [7–9], and have shown that AGA-IgG positive patients of schizophrenia could be a subgroup. Additionally, the patients with recent-onset or multi-episode schizophrenia had a higher prevalence of AGA-IgG compared with controls [10].
A study of anti-gliadin antibodies in first-episode patients with schizophrenia among a Chinese population
2019, Psychiatry ResearchCitation Excerpt :In recent years, dysfunction of the immune system has been frequently reported (Perry et al., 1979; Abi-Dargham et al., 1998; Ezeoke et al., 2013; Khandaker et al., 2015; Severance et al., 2016, 2018); GWA studies have also revealed that the strongest association signal was identified in the human leukocyte antigen (HLA) locus (International Schizophrenia Consortium et al., 2009; Schizophrenia Working Group of the Psychiatric Genomics Consortium, 2014). Interestingly, epidemiologic studies suggested that schizophrenia was very likely to be associated with wheat consumption (Graff and Handford, 1961; Dohan, 1966; Jackson et al., 2012) and a large proportion of schizophrenia patients were found to carry anti-gliadin antibodies in their circulation (Reichelt and Landmark, 1995; Dickerson et al., 2010; Cascella et al., 2011; Jin et al., 2012; Okusaga et al., 2013; Lachance and Mckenzie, 2014; McLean et al., 2017; Čiháková et al., 2018). Because most studies performed with anti-gliadin antibody test have applied the enzyme-linked immunosorbent assay (ELISA) made from the mixture of native gliadin molecules, a recent study developed an in-house ELISA with digestion-resistant peptide fragments derived from native gliadins, and they found that the change of circulating anti-gliadin antibody levels was different from previous reports (McLean et al., 2017).
No correlation between HLA-DQ 2.5, DQ 8.1 and DQ 6.2 and circulating levels of antibodies against gliadins in schizophrenia
2019, Psychiatry ResearchCitation Excerpt :Previously, we reported an increase in plasma anti-AAQ6C IgG levels in this cohort of schizophrenia patients despite lack of altered AGA IgG or IgA levels. It is worth noting that elevated AGA levels in schizophrenia have been sustained in the literature, especially in meta-analysis (Čiháková et al., 2018; Lachance and McKenzie, 2014; McLean et al., 2017). Since HLA-II molecules are crucial for the presentation of antigen to the adaptive immune system to induce the production of antibodies, the identification of HLA-associations with IgG against this γ-gliadin-derived peptide in patients with schizophrenia could strengthen the association between anti-AAQ6C IgG and schizophrenia.