The exact cause for T1D is unknown, but the contribution of genetic and environmental factors, leading to a breakdown in immune tolerance has been proposed. Genetic data strongly link the breakdown in tolerance to alterations in the transcriptional program in CD4+ T cells. Various environmental fa...
Under particular circumstances human leukocyte antigen (HLA) class I molecules may present peptides derived from extracellular proteins to CD8+ T cells (a process termed cross-presentation) to induce or maintain cytotoxic T cell responses (CTL). This interaction is likely to be important in autoi...
Tissue-specific autoimmune diseases are assumed to arise from the malfunction of two checkpoints for immune tolerance: defect in the elimination of autoreactive T-cells in the thymus, and activation of these T-cells by the corresponding autoantigens in periphery. However, evidence for this model an...
Type 1 diabetes (T1D) is a chronic disease that usually presents at childhood and affects millions of individuals worldwide. T1D is caused by T cell-mediated destruction of pancreatic beta cells, leaving affected individuals reliant on life-long exogenous insulin. It is likely that blockade of patho...
Background Gold nanoparticles (GNP) are used as a means of delivering drugs as well as proteins and peptides, particularly for cancer therapy. However, comparatively little is known regarding the use of gold nanoparticles for autoimmune disease therapy. The aim of our study was to test the effects...
T cell exhaustion is a dysfunctional state that has been associated with reduced disease activity in autoimmune disorders including type 1 diabetes (T1D). Hence, the induction of T cell exhaustion might be an attractive approach to impair self-reactive effector memory T cells and halt autoimmune ...
Background DNA including self DNA binds to Toll-like receptor 9 (TLR9) as a nucleotide-sensing receptor. TLR9 is expressed mostly on antigen presenting cells (APCs) and plays an important role in host immune response to pathogens as well as to self antigens. We have previously shown that TLR9-defici...
BACKGROUND: Antigen-specific tolerance has not yet been achieved in Type 1 diabetes (T1D) patients, who harbor diabetogenic T cells reacting against multiple beta-cell antigens. Plasmid DNA (pDNA)-encoding such antigens have been evaluated with the goal to achieve tolerance, and have the advantages ...
Introduction: Nationwide epidemiological studies show that type 1 diabetes is 3 times more prevalent in major depressed patients and first degree relatives. These individuals are also more prone to infection. The NOD mouse, a classical model for type 1 diabetes, also shows an anxious behavior, which...
Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the preclinical phase of type 1 diabetes (T1D). Little is known about the factors that influence autoantibody profiles and the continuation of the autoimmune response post-diagnosis. H...
Objectives: Microbiome studies in type 1 diabetes (T1D) to date are limited to populations of Europe (mostly North-Eastern), with one study each from Mexico, the USA, and China. We therefore sought to characterize the gut bacteriome and virome in children after onset of T1D along with age- and place...
Background: Before adaptive immune infiltration, inflammation and innate response remodels the islet to allow insulitis. The understanding of the cellular and molecular basis for the initial events would define new potential therapeutic targets. A single cell dissection of the very early phase of di...
Background: The purpose of this study was to obtain comprehensive gene expression datasets from a large number of individual islets, with defined pathological phenotypes, from organ donors with different clinical stages of type 1 diabetes. Here we will present results from an analysis that compared ...
Background: T-cell mitochondrial dysfunction has been linked with autoimmune disease. We have recently discovered that T-cells from T1D patients exhibit mitochondrial inner-membrane hyperpolarization and elevated proinflammatory function. We hypothesize that T-cells from patients with T1D display ab...
Event dates:Thursday 25 October - Monday 29 October 2018
Abstract submission deadline: Monday 14 May 2018
Abstract notification: July 2018
Early registration deadline: Monday 3 September 2018
Registration deadline: Monday 15 October 2018
Contact British Society for Immunology +44 (0)20 3019 5901 congress@immunology.org