Deficiency of invariant natural killer T cells in coeliac disease
Background: Immunoregulatory invariant natural killer (iNK) T cells rapidly produce interleukin (IL)-4 and other cytokines that suppress a Th1 response and are deficient in some autoimmune diseases. Aim: The aim of this study was to investigate any deficiency of iNK T cells in coeliac disease. Metho...
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| Veröffentlicht in: | Gut 2007-06, Vol.56 (6), p.790-795 |
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| description | Background: Immunoregulatory invariant natural killer (iNK) T cells rapidly produce interleukin (IL)-4 and other cytokines that suppress a Th1 response and are deficient in some autoimmune diseases. Aim: The aim of this study was to investigate any deficiency of iNK T cells in coeliac disease. Methods: Blood was collected from 86 subjects with coeliac disease and from 152 healthy control subjects for investigation of Vα24+ T cells by flow cytometry. iNK T cells were assessed by Vα24 and α-galactosylceramide/CD1d tetramer markers in 23 normal controls and 13 subjects with coeliac disease. Intracellular IL-4 was measured after anti-CD3 antibody stimulation. Duodenal biopsies were obtained in a subgroup of subjects with coeliac disease and control subjects for Vα24 mRNA expression using relative PCR and for Vα24+ T cells by immunofluorescence. Results: The mean numbers of circulating Vα24+ T cells and iNK T cells in coeliac disease were 27% (p |
| doi_str_mv | 10.1136/gut.2006.095307 |
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Aim: The aim of this study was to investigate any deficiency of iNK T cells in coeliac disease. Methods: Blood was collected from 86 subjects with coeliac disease and from 152 healthy control subjects for investigation of Vα24+ T cells by flow cytometry. iNK T cells were assessed by Vα24 and α-galactosylceramide/CD1d tetramer markers in 23 normal controls and 13 subjects with coeliac disease. Intracellular IL-4 was measured after anti-CD3 antibody stimulation. Duodenal biopsies were obtained in a subgroup of subjects with coeliac disease and control subjects for Vα24 mRNA expression using relative PCR and for Vα24+ T cells by immunofluorescence. Results: The mean numbers of circulating Vα24+ T cells and iNK T cells in coeliac disease were 27% (p<0.001) and 16% (p<0.001), respectively, of levels in control subjects. After in vitro anti-CD3 stimulation, numbers of IL-4+ producing iNK T cells from subjects with coeliac disease were unchanged but increased by 21% in control subjects. In subjects with coeliac disease, Vα24 mRNA intestinal expression was reduced to 17% (p<0.001) by relative PCR and numbers of intestinal Vα24+ T cells were 16% (p<0.01) of levels in control subjects. Conclusions: We conclude that Vα24+ T cells and iNK T cells are deficient in coeliac disease. We speculate that this deficiency could contribute to the failure of immunological oral tolerance that seems to underlie this disease.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>DOI: 10.1136/gut.2006.095307</identifier><identifier>PMID: 17127705</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>Adult ; Aged ; Antigens ; Antigens, Differentiation, B-Lymphocyte - analysis ; Antigens, Differentiation, B-Lymphocyte - genetics ; Autoimmune diseases ; Biological and medical sciences ; Celiac disease ; Celiac Disease - immunology ; Cells, Cultured ; Cloning ; coeliac disease ; Diabetes ; Disease ; Duodenum - immunology ; Gastroenterology ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Expression ; Gluten ; Hepatology ; Histocompatibility Antigens Class II - analysis ; Histocompatibility Antigens Class II - genetics ; Humans ; IFN ; Immunology ; Immunomodulators ; iNK T cell ; interferon ; interleukin ; Interleukin-4 - biosynthesis ; invariant natural killer T cell ; Killer Cells, Natural - immunology ; Lymphocyte Count ; Lymphocytes ; Medical sciences ; Middle Aged ; NK T cells ; Other diseases. Semiology ; Pathogenesis ; Pharmacology. Drug treatments ; RNA, Messenger - genetics ; Small Intestine ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Studies ; T cell receptors ; T-Lymphocyte Subsets - immunology ; α-galactosylceramide ; αGalCer</subject><ispartof>Gut, 2007-06, Vol.56 (6), p.790-795</ispartof><rights>Copyright 2007 by Gut</rights><rights>2007 INIST-CNRS</rights><rights>Copyright: 2007 Copyright 2007 by Gut</rights><rights>Copyright © 2007 BMJ Publishing Group & British Society of Gastroenterology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b553t-4e96ff6cea5e9fbb7776f112ae46f494064d53a4debe8142cf301b466f9a84b33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://gut.bmj.com/content/56/6/790.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://gut.bmj.com/content/56/6/790.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,723,776,780,881,3183,23550,27901,27902,53766,53768,77343,77374</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18756248$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17127705$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grose, R H</creatorcontrib><creatorcontrib>Cummins, A G</creatorcontrib><creatorcontrib>Thompson, F M</creatorcontrib><title>Deficiency of invariant natural killer T cells in coeliac disease</title><title>Gut</title><addtitle>Gut</addtitle><description>Background: Immunoregulatory invariant natural killer (iNK) T cells rapidly produce interleukin (IL)-4 and other cytokines that suppress a Th1 response and are deficient in some autoimmune diseases. Aim: The aim of this study was to investigate any deficiency of iNK T cells in coeliac disease. Methods: Blood was collected from 86 subjects with coeliac disease and from 152 healthy control subjects for investigation of Vα24+ T cells by flow cytometry. iNK T cells were assessed by Vα24 and α-galactosylceramide/CD1d tetramer markers in 23 normal controls and 13 subjects with coeliac disease. Intracellular IL-4 was measured after anti-CD3 antibody stimulation. Duodenal biopsies were obtained in a subgroup of subjects with coeliac disease and control subjects for Vα24 mRNA expression using relative PCR and for Vα24+ T cells by immunofluorescence. Results: The mean numbers of circulating Vα24+ T cells and iNK T cells in coeliac disease were 27% (p<0.001) and 16% (p<0.001), respectively, of levels in control subjects. After in vitro anti-CD3 stimulation, numbers of IL-4+ producing iNK T cells from subjects with coeliac disease were unchanged but increased by 21% in control subjects. In subjects with coeliac disease, Vα24 mRNA intestinal expression was reduced to 17% (p<0.001) by relative PCR and numbers of intestinal Vα24+ T cells were 16% (p<0.01) of levels in control subjects. Conclusions: We conclude that Vα24+ T cells and iNK T cells are deficient in coeliac disease. We speculate that this deficiency could contribute to the failure of immunological oral tolerance that seems to underlie this disease.</description><subject>Adult</subject><subject>Aged</subject><subject>Antigens</subject><subject>Antigens, Differentiation, B-Lymphocyte - analysis</subject><subject>Antigens, Differentiation, B-Lymphocyte - genetics</subject><subject>Autoimmune diseases</subject><subject>Biological and medical sciences</subject><subject>Celiac disease</subject><subject>Celiac Disease - immunology</subject><subject>Cells, Cultured</subject><subject>Cloning</subject><subject>coeliac disease</subject><subject>Diabetes</subject><subject>Disease</subject><subject>Duodenum - immunology</subject><subject>Gastroenterology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Expression</subject><subject>Gluten</subject><subject>Hepatology</subject><subject>Histocompatibility Antigens Class II - analysis</subject><subject>Histocompatibility Antigens Class II - genetics</subject><subject>Humans</subject><subject>IFN</subject><subject>Immunology</subject><subject>Immunomodulators</subject><subject>iNK T cell</subject><subject>interferon</subject><subject>interleukin</subject><subject>Interleukin-4 - biosynthesis</subject><subject>invariant natural killer T cell</subject><subject>Killer Cells, Natural - immunology</subject><subject>Lymphocyte Count</subject><subject>Lymphocytes</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>NK T cells</subject><subject>Other diseases. Semiology</subject><subject>Pathogenesis</subject><subject>Pharmacology. Drug treatments</subject><subject>RNA, Messenger - genetics</subject><subject>Small Intestine</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Studies</subject><subject>T cell receptors</subject><subject>T-Lymphocyte Subsets - immunology</subject><subject>α-galactosylceramide</subject><subject>αGalCer</subject><issn>0017-5749</issn><issn>1468-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0c9PFDEUB_DGaGQBz97MJEYPJrO0098XElwFDQQvaLg1ne4rdpntYDtD4L-3m9mAcuHUw_v05b33RegtwXNCqDi4God5g7GYY80pli_QjDChatoo9RLNMCay5pLpHbSb8wpjrJQmr9EOkaSREvMZOvoCPrgA0d1Xva9CvLUp2DhU0Q5jsl11HboOUnVROei6XEDleuiCddUyZLAZ9tErb7sMb7bvHvp5_PVi8a0--3HyfXF0Vrec06FmoIX3woHloH3bSimFJ6SxwIRnmmHBlpxatoQWFGGN8xSTlgnhtVWspXQPHU59b8Z2DUsHcSjzmZsU1jbdm94G838lht_mqr81RHOmuCgNPm4bpP7PCHkw65A3W9kI_ZhNuUdDFKfPwgYzzBhlBb5_Alf9mGK5giFSakqVbEhRB5Nyqc85gX-YmWCzSdGUFM0mRTOlWH68-3fVR7-NrYAPW2Czs51PNrqQH52SXDRMFVdPLuQB7h7qNl0bIank5vzXwlxqfXlyrE_N5-I_Tb5dr56d8i9y08Fh</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Grose, R H</creator><creator>Cummins, A G</creator><creator>Thompson, F M</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>BMJ Group</general><scope>BSCLL</scope><scope>IQODW</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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070601</creationdate><title>Deficiency of invariant natural killer T cells in coeliac disease</title><author>Grose, R H ; Cummins, A G ; Thompson, F M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b553t-4e96ff6cea5e9fbb7776f112ae46f494064d53a4debe8142cf301b466f9a84b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antigens</topic><topic>Antigens, Differentiation, B-Lymphocyte - analysis</topic><topic>Antigens, Differentiation, B-Lymphocyte - genetics</topic><topic>Autoimmune diseases</topic><topic>Biological and medical sciences</topic><topic>Celiac disease</topic><topic>Celiac Disease - immunology</topic><topic>Cells, Cultured</topic><topic>Cloning</topic><topic>coeliac disease</topic><topic>Diabetes</topic><topic>Disease</topic><topic>Duodenum - immunology</topic><topic>Gastroenterology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Expression</topic><topic>Gluten</topic><topic>Hepatology</topic><topic>Histocompatibility Antigens Class II - analysis</topic><topic>Histocompatibility Antigens Class II - genetics</topic><topic>Humans</topic><topic>IFN</topic><topic>Immunology</topic><topic>Immunomodulators</topic><topic>iNK T cell</topic><topic>interferon</topic><topic>interleukin</topic><topic>Interleukin-4 - biosynthesis</topic><topic>invariant natural killer T cell</topic><topic>Killer Cells, Natural - immunology</topic><topic>Lymphocyte Count</topic><topic>Lymphocytes</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>NK T cells</topic><topic>Other diseases. Semiology</topic><topic>Pathogenesis</topic><topic>Pharmacology. Drug treatments</topic><topic>RNA, Messenger - genetics</topic><topic>Small Intestine</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Studies</topic><topic>T cell receptors</topic><topic>T-Lymphocyte Subsets - immunology</topic><topic>α-galactosylceramide</topic><topic>αGalCer</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Grose, R H</creatorcontrib><creatorcontrib>Cummins, A G</creatorcontrib><creatorcontrib>Thompson, F M</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</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 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>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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grose, R H</au><au>Cummins, A G</au><au>Thompson, F M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficiency of invariant natural killer T cells in coeliac disease</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>56</volume><issue>6</issue><spage>790</spage><epage>795</epage><pages>790-795</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><coden>GUTTAK</coden><abstract>Background: Immunoregulatory invariant natural killer (iNK) T cells rapidly produce interleukin (IL)-4 and other cytokines that suppress a Th1 response and are deficient in some autoimmune diseases. Aim: The aim of this study was to investigate any deficiency of iNK T cells in coeliac disease. Methods: Blood was collected from 86 subjects with coeliac disease and from 152 healthy control subjects for investigation of Vα24+ T cells by flow cytometry. iNK T cells were assessed by Vα24 and α-galactosylceramide/CD1d tetramer markers in 23 normal controls and 13 subjects with coeliac disease. Intracellular IL-4 was measured after anti-CD3 antibody stimulation. Duodenal biopsies were obtained in a subgroup of subjects with coeliac disease and control subjects for Vα24 mRNA expression using relative PCR and for Vα24+ T cells by immunofluorescence. Results: The mean numbers of circulating Vα24+ T cells and iNK T cells in coeliac disease were 27% (p<0.001) and 16% (p<0.001), respectively, of levels in control subjects. After in vitro anti-CD3 stimulation, numbers of IL-4+ producing iNK T cells from subjects with coeliac disease were unchanged but increased by 21% in control subjects. In subjects with coeliac disease, Vα24 mRNA intestinal expression was reduced to 17% (p<0.001) by relative PCR and numbers of intestinal Vα24+ T cells were 16% (p<0.01) of levels in control subjects. Conclusions: We conclude that Vα24+ T cells and iNK T cells are deficient in coeliac disease. We speculate that this deficiency could contribute to the failure of immunological oral tolerance that seems to underlie this disease.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>17127705</pmid><doi>10.1136/gut.2006.095307</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Antigens Antigens, Differentiation, B-Lymphocyte - analysis Antigens, Differentiation, B-Lymphocyte - genetics Autoimmune diseases Biological and medical sciences Celiac disease Celiac Disease - immunology Cells, Cultured Cloning coeliac disease Diabetes Disease Duodenum - immunology Gastroenterology Gastroenterology. Liver. Pancreas. Abdomen Gene Expression Gluten Hepatology Histocompatibility Antigens Class II - analysis Histocompatibility Antigens Class II - genetics Humans IFN Immunology Immunomodulators iNK T cell interferon interleukin Interleukin-4 - biosynthesis invariant natural killer T cell Killer Cells, Natural - immunology Lymphocyte Count Lymphocytes Medical sciences Middle Aged NK T cells Other diseases. Semiology Pathogenesis Pharmacology. Drug treatments RNA, Messenger - genetics Small Intestine Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Studies T cell receptors T-Lymphocyte Subsets - immunology α-galactosylceramide αGalCer |
| title | Deficiency of invariant natural killer T cells in coeliac disease |
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