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      Nomenclature and listing of celiac disease relevant gluten T-cell epitopes restricted by HLA-DQ molecules

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          Abstract

          Celiac disease is caused by an abnormal intestinal T-cell response to gluten proteins of wheat, barley and rye. Over the last few years, a number of gluten T-cell epitopes restricted by celiac disease associated HLA-DQ molecules have been characterized. In this work, we give an overview of these epitopes and suggest a comprehensive, new nomenclature.

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

          L.M. Sollid, H. Gjerde, J Ek … (1989)
          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

            TS Halstensen, H Scott, T Fritz-Hansen … (1993)
            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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              The HLA-DQ2 gene dose effect in celiac disease is directly related to the magnitude and breadth of gluten-specific T cell responses.

              Dariusz Stepniak, Frits Koning, Liesbeth Spaenij … (2003)
              In patients with celiac disease, inflammatory T cell responses to HLA-DQ2-bound gluten peptides are thought to cause disease. Two types of HLA-DQ2 molecules exist, termed HLA-DQ2.5 and HLA-DQ2.2. Whereas HLA-DQ2.5 predisposes to celiac disease, HLA-DQ2.2 does not. We now provide evidence that the disease-associated HLA-DQ2.5 molecule presents a large repertoire of gluten peptides, whereas the non-disease-associated HLA-DQ2.2 molecule can present only a subset of these. Moreover, gluten presentation by HLA-DQ2 homozygous antigen-presenting cells was superior to presentation by HLA-DQ2/non-DQ2 heterozygous antigen-presenting cells in terms of T cell proliferation and cytokine secretion. Gluten presentation by HLA-DQ2.5/2.2 heterozygous antigen-presenting cells induced intermediate T cell stimulation. These results correlated with peptide binding to the antigen-presenting cells. Finally, we demonstrate that HLA-DQ trans dimers formed in HLA-DQ2.5/2.2 heterozygous individuals have properties identical with HLA-DQ2.5 dimers. Our findings explain the strongly increased risk of disease development for HLA-DQ2.5 homozygous and HLA-DQ2.2/2.5 heterozygous individuals, and they are indicative of a quantitative model for disease development, where HLA-DQ expression and the available number of T cell-stimulatory gluten peptides are critical limiting factors. This model may have important implications for disease prevention.
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                Author and article information

                Contributors
                : l.m.sollid@medisin.uio.no
                Journal
                Journal ID (nlm-ta): Immunogenetics
                Journal ID (iso-abbrev): Immunogenetics
                Title: Immunogenetics
                Publisher: Springer-Verlag (Berlin/Heidelberg )
                ISSN (Print): 0093-7711
                ISSN (Electronic): 1432-1211
                Publication date (Electronic): 10 February 2012
                Publication date PMC-release: 10 February 2012
                Publication date (Print): June 2012
                Volume: 64
                Issue: 6
                Pages: 455-460
                Affiliations
                [1 ]Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital - Rikshospitalet, Oslo, Norway
                [2 ]Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
                [3 ]Institute of Food Science, National Research Council, Avellino, Italy
                [4 ]Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, Leiden, The Netherlands
                Article
                Publisher ID: 599
                DOI: 10.1007/s00251-012-0599-z
                PMC ID: 3349865
                PubMed ID: 22322673
                SO-VID: fcddd987-fe09-491a-9376-147df67cd2ab
                Copyright © © The Author(s) 2012
                History
                Date received : 9 November 2011
                Date accepted : 13 January 2012
                Categories
                Subject: Brief Communication
                Custom metadata
                issue-copyright-statement © Springer-Verlag 2012

                ScienceOpen disciplines: Genetics
                Keywords: epitopes,hla-dq2,t cell,hla-dq8,gluten,celiac disease
                Data availability:
                ScienceOpen disciplines: Genetics
                Keywords: epitopes, hla-dq2, t cell, hla-dq8, gluten, celiac disease

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