{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["60(1)"],"submitter":["Bertin-Maghit S"],"pubmed_abstract":["Objective
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.Research design and methods
We injected RelB(lo) DCs subcutaneously into 4- or 14-week-old NOD mice and tracked the incidence of diabetes and "],"journal":["Diabetes"],"pagination":["248-57"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3012178"],"repository":["biostudies-literature"],"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."],"pmcid":["PMC3012178"],"pubmed_authors":["Pang D","Best S","Steptoe R","Bertin-Maghit S","Thomas R","Duggan E","Kay TW","Paul S","Harrison LC","Thomas H","O'Sullivan B"],"additional_accession":[]},"is_claimable":false,"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.","description":"Objective
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.Research design and methods
We injected RelB(lo) DCs subcutaneously into 4- or 14-week-old NOD mice and tracked the incidence of diabetes and ","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Jan","modification":"2025-04-20T03:57:15.172Z","creation":"2019-03-27T00:37:44Z"},"accession":"S-EPMC3012178","cross_references":{"pubmed":["20980463"],"doi":["10.2337/db10-0104"]}}