Celiac disease: how complicated can it get
In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these r...
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| Veröffentlicht in: | Immunogenetics (New York) 2010-10, Vol.62 (10), p.641-651 |
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| creator | Tjon, Jennifer May-Ling van Bergen, Jeroen Koning, Frits |
| description | In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4⁺ T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4⁺ T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma. |
| doi_str_mv | 10.1007/s00251-010-0465-9 |
| format | Article |
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While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4⁺ T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4⁺ T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.</description><identifier>ISSN: 0093-7711</identifier><identifier>EISSN: 1432-1211</identifier><identifier>DOI: 10.1007/s00251-010-0465-9</identifier><identifier>PMID: 20661732</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Adult ; Allergology ; Antigen Presentation ; Antigens ; Autoimmune diseases ; Biomedical and Life Sciences ; Biomedicine ; CD4-Positive T-Lymphocytes - immunology ; Celiac disease ; Celiac Disease - epidemiology ; Celiac Disease - genetics ; Celiac Disease - immunology ; Cell Biology ; Child ; Child, Preschool ; Cytotoxicity ; Cytotoxicity, Immunologic ; Diet ; Disease Progression ; Gene Dosage ; Gene Function ; Genetic Association Studies ; Genetic Predisposition to Disease ; Genotype ; Genotypes ; Gluten ; Glutens - immunology ; GTP-Binding Proteins ; HLA ; HLA-DQ Antigens - genetics ; HLA-DQ Antigens - immunology ; Human Genetics ; Humans ; Immunity, Mucosal ; Immunology ; Intestine, Small - immunology ; Intestine, Small - pathology ; Lymphocytes ; Lymphoma ; Lymphoma, B-Cell, Marginal Zone - etiology ; Models, Immunological ; Peptides ; Prevalence ; Proteins ; Refractory celiac disease ; Review ; Small intestine ; T cell reactivity ; T cell receptors ; Transglutaminases - physiology ; White people</subject><ispartof>Immunogenetics (New York), 2010-10, Vol.62 (10), p.641-651</ispartof><rights>The Author(s) 2010</rights><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-d49a1bb21dec41809cbfcbb26a225a0f23074999e257ff69548e8eaf858b1f2f3</citedby><cites>FETCH-LOGICAL-c492t-d49a1bb21dec41809cbfcbb26a225a0f23074999e257ff69548e8eaf858b1f2f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00251-010-0465-9$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00251-010-0465-9$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,315,782,786,887,27931,27932,41495,42564,51326</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20661732$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tjon, Jennifer May-Ling</creatorcontrib><creatorcontrib>van Bergen, Jeroen</creatorcontrib><creatorcontrib>Koning, Frits</creatorcontrib><title>Celiac disease: how complicated can it get</title><title>Immunogenetics (New York)</title><addtitle>Immunogenetics</addtitle><addtitle>Immunogenetics</addtitle><description>In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4⁺ T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4⁺ T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.</description><subject>Adult</subject><subject>Allergology</subject><subject>Antigen Presentation</subject><subject>Antigens</subject><subject>Autoimmune diseases</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Celiac disease</subject><subject>Celiac Disease - epidemiology</subject><subject>Celiac Disease - genetics</subject><subject>Celiac Disease - immunology</subject><subject>Cell Biology</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Cytotoxicity</subject><subject>Cytotoxicity, Immunologic</subject><subject>Diet</subject><subject>Disease Progression</subject><subject>Gene Dosage</subject><subject>Gene Function</subject><subject>Genetic Association Studies</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>Gluten</subject><subject>Glutens - immunology</subject><subject>GTP-Binding Proteins</subject><subject>HLA</subject><subject>HLA-DQ Antigens - genetics</subject><subject>HLA-DQ Antigens - immunology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunity, Mucosal</subject><subject>Immunology</subject><subject>Intestine, Small - immunology</subject><subject>Intestine, Small - pathology</subject><subject>Lymphocytes</subject><subject>Lymphoma</subject><subject>Lymphoma, B-Cell, Marginal Zone - etiology</subject><subject>Models, Immunological</subject><subject>Peptides</subject><subject>Prevalence</subject><subject>Proteins</subject><subject>Refractory celiac disease</subject><subject>Review</subject><subject>Small intestine</subject><subject>T cell reactivity</subject><subject>T cell receptors</subject><subject>Transglutaminases - physiology</subject><subject>White people</subject><issn>0093-7711</issn><issn>1432-1211</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kUtr3DAUhUVpaSaPH9BNa7oJBNzeq4dlZVEIQ9IWAl00WQtZliYKHmsqeRLy76PBSfpYdCXE_c6Rzj2EvEP4hADycwagAmtAqIE3olavyAI5ozVSxNdkAaBYLSXiHtnP-RYAhaLNW7JHoWlQMrogJ0s3BGOrPmRnsjutbuJ9ZeN6MwRrJtdX1oxVmKqVmw7JG2-G7I6ezgNyfXF-tfxWX_74-n15dllbruhU91wZ7DqKvbMcW1C287bcG0OpMOApA8mVUo4K6X2jBG9d64xvRduhp54dkC-z72bbrV1v3TglM-hNCmuTHnQ0Qf89GcONXsU7TRXnZSHF4PjJIMVfW5cnvQ7ZumEwo4vbrKUQJbxgO_LjP-Rt3KaxpNtBHBvBZIFwhmyKOSfnX76CoHc96LkHXXrQux60Kpr3f2Z4UTwvvgB0BnIZjSuXfr_8P9cPs8ibqM0qhayvf1JABtgqyiWwR80OmtE</recordid><startdate>20101001</startdate><enddate>20101001</enddate><creator>Tjon, Jennifer May-Ling</creator><creator>van Bergen, Jeroen</creator><creator>Koning, Frits</creator><general>Berlin/Heidelberg : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20101001</creationdate><title>Celiac disease: how complicated can it get</title><author>Tjon, Jennifer May-Ling ; van Bergen, Jeroen ; Koning, Frits</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-d49a1bb21dec41809cbfcbb26a225a0f23074999e257ff69548e8eaf858b1f2f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Allergology</topic><topic>Antigen Presentation</topic><topic>Antigens</topic><topic>Autoimmune diseases</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Celiac disease</topic><topic>Celiac Disease - epidemiology</topic><topic>Celiac Disease - genetics</topic><topic>Celiac Disease - immunology</topic><topic>Cell Biology</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Cytotoxicity</topic><topic>Cytotoxicity, Immunologic</topic><topic>Diet</topic><topic>Disease Progression</topic><topic>Gene Dosage</topic><topic>Gene Function</topic><topic>Genetic Association Studies</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>Gluten</topic><topic>Glutens - immunology</topic><topic>GTP-Binding Proteins</topic><topic>HLA</topic><topic>HLA-DQ Antigens - genetics</topic><topic>HLA-DQ Antigens - immunology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunity, Mucosal</topic><topic>Immunology</topic><topic>Intestine, Small - immunology</topic><topic>Intestine, Small - pathology</topic><topic>Lymphocytes</topic><topic>Lymphoma</topic><topic>Lymphoma, B-Cell, Marginal Zone - etiology</topic><topic>Models, Immunological</topic><topic>Peptides</topic><topic>Prevalence</topic><topic>Proteins</topic><topic>Refractory celiac disease</topic><topic>Review</topic><topic>Small intestine</topic><topic>T cell reactivity</topic><topic>T cell receptors</topic><topic>Transglutaminases - physiology</topic><topic>White people</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tjon, Jennifer May-Ling</creatorcontrib><creatorcontrib>van Bergen, Jeroen</creatorcontrib><creatorcontrib>Koning, Frits</creatorcontrib><collection>AGRIS</collection><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunogenetics (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tjon, Jennifer May-Ling</au><au>van Bergen, Jeroen</au><au>Koning, Frits</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Celiac disease: how complicated can it get</atitle><jtitle>Immunogenetics (New York)</jtitle><stitle>Immunogenetics</stitle><addtitle>Immunogenetics</addtitle><date>2010-10-01</date><risdate>2010</risdate><volume>62</volume><issue>10</issue><spage>641</spage><epage>651</epage><pages>641-651</pages><issn>0093-7711</issn><eissn>1432-1211</eissn><abstract>In the small intestine of celiac disease patients, dietary wheat gluten and similar proteins in barley and rye trigger an inflammatory response. While strict adherence to a gluten-free diet induces full recovery in most patients, a small percentage of patients fail to recover. In a subset of these refractory celiac disease patients, an (aberrant) oligoclonal intraepithelial lymphocyte population develops into overt lymphoma. Celiac disease is strongly associated with HLA-DQ2 and/or HLA-DQ8, as both genotypes predispose for disease development. This association can be explained by the fact that gluten peptides can be presented in HLA-DQ2 and HLA-DQ8 molecules on antigen presenting cells. Gluten-specific CD4⁺ T cells in the lamina propria respond to these peptides, and this likely enhances cytotoxicity of intraepithelial lymphocytes against the intestinal epithelium. We propose a threshold model for the development of celiac disease, in which the efficiency of gluten presentation to CD4⁺ T cells determines the likelihood of developing celiac disease and its complications. Key factors that influence the efficiency of gluten presentation include: (1) the level of gluten intake, (2) the enzyme tissue transglutaminase 2 which modifies gluten into high affinity binding peptides for HLA-DQ2 and HLA-DQ8, (3) the HLA-DQ type, as HLA-DQ2 binds a wider range of gluten peptides than HLA-DQ8, (4) the gene dose of HLA-DQ2 and HLA-DQ8, and finally,(5) additional genetic polymorphisms that may influence T cell reactivity. This threshold model might also help to understand the development of refractory celiac disease and lymphoma.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>20661732</pmid><doi>10.1007/s00251-010-0465-9</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Immunogenetics (New York), 2010-10, Vol.62 (10), p.641-651 |
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| subjects | Adult Allergology Antigen Presentation Antigens Autoimmune diseases Biomedical and Life Sciences Biomedicine CD4-Positive T-Lymphocytes - immunology Celiac disease Celiac Disease - epidemiology Celiac Disease - genetics Celiac Disease - immunology Cell Biology Child Child, Preschool Cytotoxicity Cytotoxicity, Immunologic Diet Disease Progression Gene Dosage Gene Function Genetic Association Studies Genetic Predisposition to Disease Genotype Genotypes Gluten Glutens - immunology GTP-Binding Proteins HLA HLA-DQ Antigens - genetics HLA-DQ Antigens - immunology Human Genetics Humans Immunity, Mucosal Immunology Intestine, Small - immunology Intestine, Small - pathology Lymphocytes Lymphoma Lymphoma, B-Cell, Marginal Zone - etiology Models, Immunological Peptides Prevalence Proteins Refractory celiac disease Review Small intestine T cell reactivity T cell receptors Transglutaminases - physiology White people |
| title | Celiac disease: how complicated can it get |
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