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      Celiac disease and HLA DQ in patients with IgA nephropathy.

      The American Journal of Gastroenterology
      Adolescent, Adult, Aged, Autoimmune Diseases, genetics, Celiac Disease, diet therapy, etiology, Child, Female, Genetic Predisposition to Disease, Glomerulonephritis, IGA, complications, HLA-DQ Antigens, Haplotypes, Humans, Male, Middle Aged

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          Abstract

          Despite some reports on an association between celiac disease and IgA nephropathy, the evidence is still sparse. Celiac disease is strongly associated with the HLA DQ2 and DQ8 haplotypes, which might explain the potential risk of patients to contract various autoimmune conditions. In this study, we sought to establish how common celiac disease is in patients with IgA nephropathy, and whether the possible association can be explained by similar HLA DQ status. A total of 223 consecutive adult patients with IgA nephropathy were studied; 95 cadaver organ transplant donors served as controls for HLA DQ analysis. The diagnosis of celiac disease was based on small bowel mucosal biopsy. All known celiac cases were recorded, and eligible patients (n = 168) underwent serological screening for celiac disease as well as HLA DQ2 and DQ8 analysis. Screening methods were serum endomysium and tissue transglutaminase antibodies; patients who tested positive underwent mucosal biopsy. Eight patients (3.6%, 95% CI = 1.6-7.0%) with IgA nephropathy were found to have celiac disease; three of them were identified by serological screening. All celiac cases had the HLA DQ2 or DQ8 haplotype, but these were not more common in patients with IgA nephropathy than in controls. As many as 14% of HLA DQ2 positive patients with IgA nephropathy had celiac disease. Gluten-free diet had no apparent influence on the course of nephropathy. Although there is no increase in celiac-type HLA DQ, patients with IgA nephropathy carry a risk of contracting celiac disease. It can be hypothesized that the increased intestinal permeability in IgA nephropathy may predispose genetically susceptible patients to celiac disease.

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          Gluten, major histocompatibility complex, and the small intestine

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            Evidence for a primary association of celiac disease to a particular HLA-DQ alpha/beta heterodimer

            Typing of DNA from 94 unrelated children with celiac disease (CD) with HLA-DQA1 and -DQB1 allele-specific oligonucleotide probes revealed that all but one (i.e., 98.9%) may share a particular combination of a DQA1 and a DQB1 gene. These genes are arranged in cis position on the DR3DQw2 haplotype and in trans position in DR5DQw7/DR7DQw2 heterozygous individuals. Thus, most CD patients may share the same cis- or trans- encoded HLA-DQ alpha/beta heterodimer.
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              Gliadin-specific, HLA-DQ(alpha 1*0501,beta 1*0201) restricted T cells isolated from the small intestinal mucosa of celiac disease patients

              Celiac disease (CD) is most probably an immunological disease, precipitated in susceptible individuals by ingestion of wheat gliadin and related proteins from other cereals. The disease shows a strong human HLA association predominantly to the cis or trans encoded HLA- DQ(alpha 1*0501,beta 1*0201) (DQ2) heterodimer. T cell recognition of gliadin presented by this DQ heterodimer may thus be of immunopathogenic importance in CD. We therefore challenged small intestinal biopsies from adult CD patients on a gluten-free diet in vitro with gluten (containing both gliadin and other wheat proteins), and isolated activated CD25+ T cells. Polyclonal T cell lines and a panel of T cell clones recognizing gluten were established. They recognized the gliadin moiety of gluten, but not proteins from other cereals. Inhibition studies with anti-HLA antibodies demonstrated predominant antigen presentation by HLA-DQ molecules. The main antigen- presenting molecule was established to be the CD-associated DQ(alpha 1*0501, beta 1*0201) heterodimer. The gluten-reactive T cell clones were CD4+, CD8-, and carried diverse combinations of T cell receptor (TCR) V alpha and V beta chains. The findings suggest preferential mucosal presentation of gluten-derived peptides by HLA-DQ(alpha 1*0501, beta 1*0201) in CD, which may explain the HLA association.
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