<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Krischer JP</submitter><funding>National Center for Advancing Translational Sciences</funding><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>National Institute of Diabetes and Digestive and Kidney Diseases</funding><funding>National Institutes of Health</funding><pagination>1194-1202</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5566280</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(9)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>We tested the associations between genetic background and selected environmental exposures with respect to islet autoantibodies and type 1 diabetes.&lt;h4>Research design and methods&lt;/h4>Infants with HLA-DR high-risk genotypes were prospectively followed for diabetes-related autoantibodies. Single nucleotide polymorphisms (SNPs) came from the Illumina ImmunoChip and environmental exposure data were by parental report. Children were followed to age 6 years.&lt;h4>Results&lt;/h4>Insulin autoantibodies occurred earlier than GAD antibody (GADA) and then declined, while GADA incidence rose and remained constant (significant in HLA-DR4 but not in the DR3/3 children). The presence of SNPs rs2476601 (&lt;i>PTPN22&lt;/i>) and rs2292239 (&lt;i>ERBB3&lt;/i>) demonstrated increased risk of both autoantib</pubmed_abstract><journal>Diabetes care</journal><pubmed_title>Genetic and Environmental Interactions Modify the Risk of Diabetes-Related Autoimmunity by 6 Years of Age: The TEDDY Study.</pubmed_title><pmcid>PMC5566280</pmcid><funding_grant_id>U01 DK063861</funding_grant_id><funding_grant_id>UC4 DK063836</funding_grant_id><funding_grant_id>UC4-DK-63829</funding_grant_id><funding_grant_id>UC4 DK117483</funding_grant_id><funding_grant_id>UC4-DK-95300</funding_grant_id><funding_grant_id>U01 DK063821</funding_grant_id><funding_grant_id>U01 DK063865</funding_grant_id><funding_grant_id>UL1 TR001427</funding_grant_id><funding_grant_id>U01 DK063863</funding_grant_id><funding_grant_id>U01-DK-63790</funding_grant_id><funding_grant_id>UC4-DK-63836</funding_grant_id><funding_grant_id>UC4 DK112243</funding_grant_id><funding_grant_id>U01-DK-63836</funding_grant_id><funding_grant_id>UC4 DK095300</funding_grant_id><funding_grant_id>UL1 TR000064</funding_grant_id><funding_grant_id>U01-DK-63829</funding_grant_id><funding_grant_id>U01 DK063790</funding_grant_id><funding_grant_id>UC4 DK063863</funding_grant_id><funding_grant_id>UC4 DK063865</funding_grant_id><funding_grant_id>UC4 DK063821</funding_grant_id><funding_grant_id>U01 DK063836</funding_grant_id><funding_grant_id>UC4 DK063861</funding_grant_id><funding_grant_id>UC4 DK100238</funding_grant_id><funding_grant_id>UC4 DK106955</funding_grant_id><funding_grant_id>UC4-DK-63861</funding_grant_id><funding_grant_id>U01 DK063829</funding_grant_id><funding_grant_id>U01-DK-63861</funding_grant_id><funding_grant_id>HHSN267200700014C</funding_grant_id><funding_grant_id>U01-DK-63863</funding_grant_id><funding_grant_id>U01-DK-63865</funding_grant_id><funding_grant_id>U01-DK-63821</funding_grant_id><funding_grant_id>UC4-DK-63865</funding_grant_id><funding_grant_id>UC4-DK-63821</funding_grant_id><funding_grant_id>UL1 TR001082</funding_grant_id><funding_grant_id>UC4-DK-63863</funding_grant_id><funding_grant_id>UC4 DK063829</funding_grant_id><pubmed_authors>Krischer JP</pubmed_authors><pubmed_authors>Hagopian WA</pubmed_authors><pubmed_authors>She JX</pubmed_authors><pubmed_authors>Ziegler AG</pubmed_authors><pubmed_authors>TEDDY Study Group</pubmed_authors><pubmed_authors>Lynch KF</pubmed_authors><pubmed_authors>Rewers MJ</pubmed_authors><pubmed_authors>Akolkar B</pubmed_authors><pubmed_authors>Toppari J</pubmed_authors><pubmed_authors>Lernmark A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genetic and Environmental Interactions Modify the Risk of Diabetes-Related Autoimmunity by 6 Years of Age: The TEDDY Study.</name><description>&lt;h4>Objective&lt;/h4>We tested the associations between genetic background and selected environmental exposures with respect to islet autoantibodies and type 1 diabetes.&lt;h4>Research design and methods&lt;/h4>Infants with HLA-DR high-risk genotypes were prospectively followed for diabetes-related autoantibodies. Single nucleotide polymorphisms (SNPs) came from the Illumina ImmunoChip and environmental exposure data were by parental report. Children were followed to age 6 years.&lt;h4>Results&lt;/h4>Insulin autoantibodies occurred earlier than GAD antibody (GADA) and then declined, while GADA incidence rose and remained constant (significant in HLA-DR4 but not in the DR3/3 children). The presence of SNPs rs2476601 (&lt;i>PTPN22&lt;/i>) and rs2292239 (&lt;i>ERBB3&lt;/i>) demonstrated increased risk of both autoantib</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Sep</publication><modification>2026-05-04T16:15:26.391Z</modification><creation>2019-03-26T23:53:49Z</creation></dates><accession>S-EPMC5566280</accession><cross_references><pubmed>28646072</pubmed><doi>10.2337/dc17-0238</doi></cross_references></HashMap>