<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>60(1)</volume><submitter>Bertin-Maghit S</submitter><pubmed_abstract>&lt;h4>Objective&lt;/h4>The effectiveness of tolerizing immunotherapeutic strategies, such as anti-CD40L or dendritic cells (DCs), is greater when administered to young nonobese diabetic (NOD) mice than at peak insulitis. RelB(lo) DCs, generated in the presence of an nuclear factor-κB inhibitor, induce T-regulatory (Treg) cells and suppress inflammation in a model of rheumatoid arthritis. Interleukin (IL)-1β is overexpressed in humans and mice at risk of type 1 diabetes, dysregulates Treg cells, and accelerates diabetes in NOD mice. We investigated the relationship between IL-1β production and the response to RelB(lo) DCs in the prediabetic period.&lt;h4>Research design and methods&lt;/h4>We injected RelB(lo) DCs subcutaneously into 4- or 14-week-old NOD mice and tracked the incidence of diabetes and </pubmed_abstract><journal>Diabetes</journal><pagination>248-57</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3012178</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Interleukin-1β produced in response to islet autoantigen presentation differentiates T-helper 17 cells at the expense of regulatory T-cells: Implications for the timing of tolerizing immunotherapy.</pubmed_title><pmcid>PMC3012178</pmcid><pubmed_authors>Pang D</pubmed_authors><pubmed_authors>Best S</pubmed_authors><pubmed_authors>Steptoe R</pubmed_authors><pubmed_authors>Bertin-Maghit S</pubmed_authors><pubmed_authors>Thomas R</pubmed_authors><pubmed_authors>Duggan E</pubmed_authors><pubmed_authors>Kay TW</pubmed_authors><pubmed_authors>Paul S</pubmed_authors><pubmed_authors>Harrison LC</pubmed_authors><pubmed_authors>Thomas H</pubmed_authors><pubmed_authors>O'Sullivan B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Interleukin-1β produced in response to islet autoantigen presentation differentiates T-helper 17 cells at the expense of regulatory T-cells: Implications for the timing of tolerizing immunotherapy.</name><description>&lt;h4>Objective&lt;/h4>The effectiveness of tolerizing immunotherapeutic strategies, such as anti-CD40L or dendritic cells (DCs), is greater when administered to young nonobese diabetic (NOD) mice than at peak insulitis. RelB(lo) DCs, generated in the presence of an nuclear factor-κB inhibitor, induce T-regulatory (Treg) cells and suppress inflammation in a model of rheumatoid arthritis. Interleukin (IL)-1β is overexpressed in humans and mice at risk of type 1 diabetes, dysregulates Treg cells, and accelerates diabetes in NOD mice. We investigated the relationship between IL-1β production and the response to RelB(lo) DCs in the prediabetic period.&lt;h4>Research design and methods&lt;/h4>We injected RelB(lo) DCs subcutaneously into 4- or 14-week-old NOD mice and tracked the incidence of diabetes and </description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jan</publication><modification>2025-04-20T03:57:15.172Z</modification><creation>2019-03-27T00:37:44Z</creation></dates><accession>S-EPMC3012178</accession><cross_references><pubmed>20980463</pubmed><doi>10.2337/db10-0104</doi></cross_references></HashMap>