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The external world of gluten and autoimmunity
In a simplistic way, antigens encountered on a mucosal surface trigger a Th2 (sometimes and depending on the authors Th3 or T regulatory) type of response instead of a proinflammatory Th1 response, dominant in autoimmune diseases. 4 This mucosal characteristic has been exploited to protect or even t...
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Published in: | Gut 2001-10, Vol.49 (4), p.463-464 |
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description | In a simplistic way, antigens encountered on a mucosal surface trigger a Th2 (sometimes and depending on the authors Th3 or T regulatory) type of response instead of a proinflammatory Th1 response, dominant in autoimmune diseases. 4 This mucosal characteristic has been exploited to protect or even treat autoimmune diseases via induction of mucosal tolerance. 5 Some gastrointestinal diseases are associated with autoimmunity but coeliac disease (CD) has two important characteristics that make it a cut above the rest: the strongest HLA association and a single well defined trigger-gluten. 6 CD itself is a "spurious" autoimmune disease as it induces a reaction against self (antibodies against tissue transglutaminase) but this self aggression resolves on gluten withdrawal and hence strictly speaking does not qualify as an autoimmune disease. Because we can control the encounter with the environmental factor (gluten) in CD, this is an ideal condition to study the relevance of the environment in induction of autoimmunity. [...]we have to clarify why these late diagnosed patients are more prone to develop autoimmunity and how they differ compared with early diagnosed patients if we want to "make sense" of this finding. [...]functional, epidemiological, as well as genetic studies are required to unravel this puzzling question to shed light on the nature of the link between CD and autoimmune diseases and possibly to autoimmunity itself. |
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Because we can control the encounter with the environmental factor (gluten) in CD, this is an ideal condition to study the relevance of the environment in induction of autoimmunity. [...]we have to clarify why these late diagnosed patients are more prone to develop autoimmunity and how they differ compared with early diagnosed patients if we want to "make sense" of this finding. 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Because we can control the encounter with the environmental factor (gluten) in CD, this is an ideal condition to study the relevance of the environment in induction of autoimmunity. [...]we have to clarify why these late diagnosed patients are more prone to develop autoimmunity and how they differ compared with early diagnosed patients if we want to "make sense" of this finding. [...]functional, epidemiological, as well as genetic studies are required to unravel this puzzling question to shed light on the nature of the link between CD and autoimmune diseases and possibly to autoimmunity itself.</description><subject>Age</subject><subject>Analysis</subject><subject>Animals</subject><subject>Autoimmune diseases</subject><subject>Autoimmune Diseases - genetics</subject><subject>Autoimmune Diseases - immunology</subject><subject>Celiac disease</subject><subject>Celiac Disease - genetics</subject><subject>Celiac Disease - immunology</subject><subject>Comorbidity</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Disease</subject><subject>Diseases in Twins</subject><subject>Environmental Exposure</subject><subject>Genetic disorders</subject><subject>Gluten</subject><subject>Glutens - immunology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Patients</subject><subject>Twins, Monozygotic</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNp9kc1rFDEYh4Modl29eZZBD16cNZl8Xwpla1uhVITqwUvIZN6ZZp1J6nzU9r83wy79gEVyCOR9eH68-SH0luAVIVR8bqZxxfSKrZigz9CCMKFyWij1HC0wJjLnkukD9GoYNhhjpTR5iQ4I4VwLqhcov7yCDG5H6INts7-xb6ss1lnTTiOEzIYqs9MYfddNwY93r9GL2rYDvNndS_Tj5Mvl-iw__3b6dX10npdc4TF3zPLSYV1UFdSO1Vjb2gLBFQWlgBXEaS4EEFYWllKmiNYlk8oxxWzpqKJLdLj1Xk9lB5WDMPa2Nde972x_Z6L15ukk-CvTxBtDZKGYKJLgw07Qxz8TDKPZxGlecUiI1Jrhef8ler-lGtuC8aGOSeY6PzhzJDXnQqpZ9WkP1ECAFBwD1D49P8bzPXg6FXTe7eN3etfHYeihvt-SYDMXbFLBhmnDTCo44e8e_8wDvGv0Id8PI9zez23_2whJJTcXP9fm-6-1ONYn0sz5H7d82W3-H_0PfrK73w</recordid><startdate>20011001</startdate><enddate>20011001</enddate><creator>LONDEI, M</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</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>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20011001</creationdate><title>The external world of gluten and autoimmunity</title><author>LONDEI, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b580t-c4a5bc092ddefc4f09afae10d3e88e421c9566e14b2a3348199b478c484abc383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Age</topic><topic>Analysis</topic><topic>Animals</topic><topic>Autoimmune diseases</topic><topic>Autoimmune Diseases - genetics</topic><topic>Autoimmune Diseases - immunology</topic><topic>Celiac disease</topic><topic>Celiac Disease - genetics</topic><topic>Celiac Disease - immunology</topic><topic>Comorbidity</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Disease</topic><topic>Diseases in Twins</topic><topic>Environmental Exposure</topic><topic>Genetic disorders</topic><topic>Gluten</topic><topic>Glutens - immunology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Patients</topic><topic>Twins, Monozygotic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>LONDEI, M</creatorcontrib><collection>Istex</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM 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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</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>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>LONDEI, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The external world of gluten and autoimmunity</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2001-10-01</date><risdate>2001</risdate><volume>49</volume><issue>4</issue><spage>463</spage><epage>464</epage><pages>463-464</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract>In a simplistic way, antigens encountered on a mucosal surface trigger a Th2 (sometimes and depending on the authors Th3 or T regulatory) type of response instead of a proinflammatory Th1 response, dominant in autoimmune diseases. 4 This mucosal characteristic has been exploited to protect or even treat autoimmune diseases via induction of mucosal tolerance. 5 Some gastrointestinal diseases are associated with autoimmunity but coeliac disease (CD) has two important characteristics that make it a cut above the rest: the strongest HLA association and a single well defined trigger-gluten. 6 CD itself is a "spurious" autoimmune disease as it induces a reaction against self (antibodies against tissue transglutaminase) but this self aggression resolves on gluten withdrawal and hence strictly speaking does not qualify as an autoimmune disease. Because we can control the encounter with the environmental factor (gluten) in CD, this is an ideal condition to study the relevance of the environment in induction of autoimmunity. [...]we have to clarify why these late diagnosed patients are more prone to develop autoimmunity and how they differ compared with early diagnosed patients if we want to "make sense" of this finding. [...]functional, epidemiological, as well as genetic studies are required to unravel this puzzling question to shed light on the nature of the link between CD and autoimmune diseases and possibly to autoimmunity itself.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>11559639</pmid><doi>10.1136/gut.49.4.463</doi><tpages>2</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Age Analysis Animals Autoimmune diseases Autoimmune Diseases - genetics Autoimmune Diseases - immunology Celiac disease Celiac Disease - genetics Celiac Disease - immunology Comorbidity Complications and side effects Development and progression Diabetes Disease Diseases in Twins Environmental Exposure Genetic disorders Gluten Glutens - immunology Health aspects Humans Mice Mice, Inbred NOD Patients Twins, Monozygotic |
title | The external world of gluten and autoimmunity |
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