Pre-diagnostic genotyping identifies T1D subjects with impaired Treg IL-2 signaling and an elevated proportion of FOXP3+IL-17+ cells
T-regulatory cells (Tregs) are essential for immune tolerance, and animal studies implicate their dysfunction in type 1 diabetes (T1D) pathogenesis. Tregs require interleukin-2 (IL-2) for their suppressive function, and variants in IL-2/IL-2R pathway genes have been associated with T1D. We previousl...
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| Veröffentlicht in: | Genes and immunity 2017, Vol.18 (1), p.15-21 |
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| creator | Marwaha, A K Panagiotopoulos, C Biggs, C M Staiger, S Del Bel, K L Hirschfeld, A F Priatel, J J Turvey, S E Tan, R |
| description | T-regulatory cells (Tregs) are essential for immune tolerance, and animal studies implicate their dysfunction in type 1 diabetes (T1D) pathogenesis. Tregs require interleukin-2 (IL-2) for their suppressive function, and variants in IL-2/IL-2R pathway genes have been associated with T1D. We previously reported that recent-onset T1D subjects have an increased population of FOXP3
lo
Tregs that secrete the pro-inflammatory cytokine, interleukin-17 (IL-17). We hypothesize that IL-2 signaling defects may drive T1D development by skewing protective Tregs towards an inflammatory Th17 phenotype. Overall, we found that the proportion of FOXP3
+
IL-17
+
cells in T1D subjects pre-diagnosis was unchanged compared with healthy controls. However, stratification by
IL2RA
single-nucleotide polymorphisms revealed that T1D subjects with the rs3118470 CC risk variant have Tregs with IL-2 signaling defects and an increased proportion of FOXP3
+
IL-17
+
cells before diagnosis. These data suggest a potential mechanism for genetically controlled loss of Treg function via dysfunctional IL-2 signaling in T1D. |
| doi_str_mv | 10.1038/gene.2016.44 |
| format | Article |
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lo
Tregs that secrete the pro-inflammatory cytokine, interleukin-17 (IL-17). We hypothesize that IL-2 signaling defects may drive T1D development by skewing protective Tregs towards an inflammatory Th17 phenotype. Overall, we found that the proportion of FOXP3
+
IL-17
+
cells in T1D subjects pre-diagnosis was unchanged compared with healthy controls. However, stratification by
IL2RA
single-nucleotide polymorphisms revealed that T1D subjects with the rs3118470 CC risk variant have Tregs with IL-2 signaling defects and an increased proportion of FOXP3
+
IL-17
+
cells before diagnosis. These data suggest a potential mechanism for genetically controlled loss of Treg function via dysfunctional IL-2 signaling in T1D.</description><identifier>ISSN: 1466-4879</identifier><identifier>ISSN: 1476-5470</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/gene.2016.44</identifier><identifier>PMID: 28053319</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/31 ; 38 ; 631/208/728 ; 631/250/2152 ; Biomarkers - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Comparative analysis ; Cytokines ; Diabetes ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Type 1 - diagnosis ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Diagnosis ; Flow Cytometry ; Forkhead Transcription Factors - genetics ; Foxp3 protein ; Gene Expression ; Genes ; Genetic aspects ; Genotype ; Genotype & phenotype ; Genotyping ; Health aspects ; Helper cells ; Human Genetics ; Humans ; Immune Tolerance ; Immunological tolerance ; Immunology ; Immunoregulation ; Inflammation ; Interleukin 17 ; Interleukin 2 ; Interleukin 2 receptors ; Interleukin-17 - genetics ; Interleukin-2 - genetics ; Interleukins ; Lymphocytes ; Lymphocytes T ; original-article ; Pathogenesis ; Pathology ; Pediatrics ; Phenotypes ; Phosphorylation ; Physiological aspects ; Prognosis ; Signal Transduction ; Single nucleotide polymorphisms ; Single-nucleotide polymorphism ; Suppressor cells ; T-Lymphocytes, Regulatory - immunology ; Th17 Cells ; Type 1 diabetes ; Variance analysis</subject><ispartof>Genes and immunity, 2017, Vol.18 (1), p.15-21</ispartof><rights>Macmillan Publishers Limited, part of Springer Nature. 2017</rights><rights>COPYRIGHT 2017 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2017</rights><rights>Macmillan Publishers Limited, part of Springer Nature. 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4944-3cdd3363d099cb83b713179d21b0cefdbb71bff4b7055190fe8ef50e3cebf1a23</citedby><cites>FETCH-LOGICAL-c4944-3cdd3363d099cb83b713179d21b0cefdbb71bff4b7055190fe8ef50e3cebf1a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gene.2016.44$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gene.2016.44$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28053319$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marwaha, A K</creatorcontrib><creatorcontrib>Panagiotopoulos, C</creatorcontrib><creatorcontrib>Biggs, C M</creatorcontrib><creatorcontrib>Staiger, S</creatorcontrib><creatorcontrib>Del Bel, K L</creatorcontrib><creatorcontrib>Hirschfeld, A F</creatorcontrib><creatorcontrib>Priatel, J J</creatorcontrib><creatorcontrib>Turvey, S E</creatorcontrib><creatorcontrib>Tan, R</creatorcontrib><title>Pre-diagnostic genotyping identifies T1D subjects with impaired Treg IL-2 signaling and an elevated proportion of FOXP3+IL-17+ cells</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>T-regulatory cells (Tregs) are essential for immune tolerance, and animal studies implicate their dysfunction in type 1 diabetes (T1D) pathogenesis. Tregs require interleukin-2 (IL-2) for their suppressive function, and variants in IL-2/IL-2R pathway genes have been associated with T1D. We previously reported that recent-onset T1D subjects have an increased population of FOXP3
lo
Tregs that secrete the pro-inflammatory cytokine, interleukin-17 (IL-17). We hypothesize that IL-2 signaling defects may drive T1D development by skewing protective Tregs towards an inflammatory Th17 phenotype. Overall, we found that the proportion of FOXP3
+
IL-17
+
cells in T1D subjects pre-diagnosis was unchanged compared with healthy controls. However, stratification by
IL2RA
single-nucleotide polymorphisms revealed that T1D subjects with the rs3118470 CC risk variant have Tregs with IL-2 signaling defects and an increased proportion of FOXP3
+
IL-17
+
cells before diagnosis. These data suggest a potential mechanism for genetically controlled loss of Treg function via dysfunctional IL-2 signaling in T1D.</description><subject>13/31</subject><subject>38</subject><subject>631/208/728</subject><subject>631/250/2152</subject><subject>Biomarkers - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Comparative analysis</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - diagnosis</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diagnosis</subject><subject>Flow Cytometry</subject><subject>Forkhead Transcription Factors - genetics</subject><subject>Foxp3 protein</subject><subject>Gene Expression</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Genotyping</subject><subject>Health aspects</subject><subject>Helper cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immune Tolerance</subject><subject>Immunological tolerance</subject><subject>Immunology</subject><subject>Immunoregulation</subject><subject>Inflammation</subject><subject>Interleukin 17</subject><subject>Interleukin 2</subject><subject>Interleukin 2 receptors</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-2 - genetics</subject><subject>Interleukins</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>original-article</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Pediatrics</subject><subject>Phenotypes</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Prognosis</subject><subject>Signal Transduction</subject><subject>Single nucleotide polymorphisms</subject><subject>Single-nucleotide polymorphism</subject><subject>Suppressor cells</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>Th17 Cells</subject><subject>Type 1 diabetes</subject><subject>Variance analysis</subject><issn>1466-4879</issn><issn>1476-5470</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9ktFrFDEQxhdRbK2--SwBX5S6Z7LJ7iYvQqlWDw5a9ATfQjY72ebYS9Zkt9p3_3CzXK09KRJCwszv-5IZJsueE7wgmPK3HThYFJhUC8YeZIeE1VVesho_nO9VlTNei4PsSYwbnCBSicfZQcFxSSkRh9mviwB5a1XnfBytRsnNj9eDdR2yLbjRGgsRrcl7FKdmA3qM6IcdL5HdDsoGaNE6QIeWq7xA0XZO9bNSuTZtBD1cqTExQ_CDD6P1DnmDzs6_XdDjJCH1MdLQ9_Fp9sioPsKzm_Mo-3r2YX36KV-df1yenqxyzQRjOdVtS2lFWyyEbjhtakJJLdqCNFiDaZsUaIxhTY3LkghsgIMpMVANjSGqoEfZu53vMDVbaHWqL6heDsFuVbiWXlm5n3H2Unb-SpacUVbTZPDqxiD47xPEUW5tnEtQDvwUJeFlWfOKVyKhL_9BN34KqUFRFhUpS4qLmv2PIrwinFBRVX-pTvUgrTM-_U7PT8sTVnNRFkTM1OIeKq0WtlZ7B8am-J7g9Z4gMSP8HDs1xSiXXz7vs292rA4-xgDmtmsEy3kO5TyHcp5Dyea6Xtzt9C38Z_ASkO-AmFKug3Cn8PsMfwM9ZuXe</recordid><startdate>2017</startdate><enddate>2017</enddate><creator>Marwaha, A K</creator><creator>Panagiotopoulos, C</creator><creator>Biggs, C M</creator><creator>Staiger, S</creator><creator>Del Bel, K L</creator><creator>Hirschfeld, A F</creator><creator>Priatel, J J</creator><creator>Turvey, S E</creator><creator>Tan, R</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>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>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2017</creationdate><title>Pre-diagnostic genotyping identifies T1D subjects with impaired Treg IL-2 signaling and an elevated proportion of FOXP3+IL-17+ cells</title><author>Marwaha, A K ; Panagiotopoulos, C ; Biggs, C M ; Staiger, S ; Del Bel, K L ; Hirschfeld, A F ; Priatel, J J ; Turvey, S E ; Tan, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4944-3cdd3363d099cb83b713179d21b0cefdbb71bff4b7055190fe8ef50e3cebf1a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>13/31</topic><topic>38</topic><topic>631/208/728</topic><topic>631/250/2152</topic><topic>Biomarkers - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Comparative analysis</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Type 1 - diagnosis</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diagnosis</topic><topic>Flow Cytometry</topic><topic>Forkhead Transcription Factors - genetics</topic><topic>Foxp3 protein</topic><topic>Gene Expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Genotyping</topic><topic>Health aspects</topic><topic>Helper cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immune Tolerance</topic><topic>Immunological tolerance</topic><topic>Immunology</topic><topic>Immunoregulation</topic><topic>Inflammation</topic><topic>Interleukin 17</topic><topic>Interleukin 2</topic><topic>Interleukin 2 receptors</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-2 - genetics</topic><topic>Interleukins</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>original-article</topic><topic>Pathogenesis</topic><topic>Pathology</topic><topic>Pediatrics</topic><topic>Phenotypes</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Prognosis</topic><topic>Signal Transduction</topic><topic>Single nucleotide polymorphisms</topic><topic>Single-nucleotide polymorphism</topic><topic>Suppressor cells</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>Th17 Cells</topic><topic>Type 1 diabetes</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marwaha, A K</creatorcontrib><creatorcontrib>Panagiotopoulos, C</creatorcontrib><creatorcontrib>Biggs, C M</creatorcontrib><creatorcontrib>Staiger, S</creatorcontrib><creatorcontrib>Del Bel, K L</creatorcontrib><creatorcontrib>Hirschfeld, A F</creatorcontrib><creatorcontrib>Priatel, J J</creatorcontrib><creatorcontrib>Turvey, S E</creatorcontrib><creatorcontrib>Tan, R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology 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>Public Health Database</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>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>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>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marwaha, A K</au><au>Panagiotopoulos, C</au><au>Biggs, C M</au><au>Staiger, S</au><au>Del Bel, K L</au><au>Hirschfeld, A F</au><au>Priatel, J J</au><au>Turvey, S E</au><au>Tan, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pre-diagnostic genotyping identifies T1D subjects with impaired Treg IL-2 signaling and an elevated proportion of FOXP3+IL-17+ cells</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2017</date><risdate>2017</risdate><volume>18</volume><issue>1</issue><spage>15</spage><epage>21</epage><pages>15-21</pages><issn>1466-4879</issn><issn>1476-5470</issn><eissn>1476-5470</eissn><abstract>T-regulatory cells (Tregs) are essential for immune tolerance, and animal studies implicate their dysfunction in type 1 diabetes (T1D) pathogenesis. Tregs require interleukin-2 (IL-2) for their suppressive function, and variants in IL-2/IL-2R pathway genes have been associated with T1D. We previously reported that recent-onset T1D subjects have an increased population of FOXP3
lo
Tregs that secrete the pro-inflammatory cytokine, interleukin-17 (IL-17). We hypothesize that IL-2 signaling defects may drive T1D development by skewing protective Tregs towards an inflammatory Th17 phenotype. Overall, we found that the proportion of FOXP3
+
IL-17
+
cells in T1D subjects pre-diagnosis was unchanged compared with healthy controls. However, stratification by
IL2RA
single-nucleotide polymorphisms revealed that T1D subjects with the rs3118470 CC risk variant have Tregs with IL-2 signaling defects and an increased proportion of FOXP3
+
IL-17
+
cells before diagnosis. These data suggest a potential mechanism for genetically controlled loss of Treg function via dysfunctional IL-2 signaling in T1D.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28053319</pmid><doi>10.1038/gene.2016.44</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Genes and immunity, 2017, Vol.18 (1), p.15-21 |
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| source | MEDLINE; SpringerLink Journals |
| subjects | 13/31 38 631/208/728 631/250/2152 Biomarkers - metabolism Biomedical and Life Sciences Biomedicine Cancer Research Comparative analysis Cytokines Diabetes Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - diagnosis Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diagnosis Flow Cytometry Forkhead Transcription Factors - genetics Foxp3 protein Gene Expression Genes Genetic aspects Genotype Genotype & phenotype Genotyping Health aspects Helper cells Human Genetics Humans Immune Tolerance Immunological tolerance Immunology Immunoregulation Inflammation Interleukin 17 Interleukin 2 Interleukin 2 receptors Interleukin-17 - genetics Interleukin-2 - genetics Interleukins Lymphocytes Lymphocytes T original-article Pathogenesis Pathology Pediatrics Phenotypes Phosphorylation Physiological aspects Prognosis Signal Transduction Single nucleotide polymorphisms Single-nucleotide polymorphism Suppressor cells T-Lymphocytes, Regulatory - immunology Th17 Cells Type 1 diabetes Variance analysis |
| title | Pre-diagnostic genotyping identifies T1D subjects with impaired Treg IL-2 signaling and an elevated proportion of FOXP3+IL-17+ cells |
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