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https://www.selleckchem.com/products/ipi-145-ink1197.html Aims/hypothesis Self-antigen-specific T cell responses drive type 1 diabetes pathogenesis, but alterations in innate immune responses are also critical and not as well understood. Innate immunity in human type 1 diabetes has primarily been assessed via gene-expression analysis of unstimulated peripheral blood mononuclear cells, without the immune activation that could amplify disease-associated signals. Increased responsiveness in each of the two main innate immune pathways, driven by either type 1 IFN (IFN-1) or IL-1, have been detected in type 1 diabetes, but the dominant innate pathway is still unclear. This study aimed to determine the key innate pathway in type 1 diabetes and assess the whole blood immune stimulation assay as a tool to investigate this. Methods The TruCulture whole blood ex vivo stimulation assay, paired with gene expression and cytokine measurements, was used to characterise changes in the stimulated innate immune response in type 1 diabetes. We applied specific cytokine-induced signatuestablished type 1 diabetes. A stimulated IFN-1 gene signature may be a potential biomarker for type 1 diabetes and used to evaluate the effects of therapies targeting this pathway. Data availability Mouse gene expression data are found in the gene expression omnibus (GEO) repository, accession GSE146452 (www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146452). Nanostring count data from the human experiments were deposited in the GEO repository, accession GSE146338 (www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE146338). Data files and R code for all analyses are available at https//github.com/rodriguesk/T1D_truculture_diabetologia. Graphical abstract.With increasing survival trends for children and adolescents with congenital heart defects (CHD), there is a growing need to focus on transition from pediatric to adult specialty cardiac care. To better understand parental perspectives on the transition proces

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