Abstract
The first Fresh Ideas, Foundational Experiments (FIFE): Immunology and Diabetes symposia workshop took place in 2016 and exemplified the active interest of a number of several investigators interested the global rise in the incidence of type 1 diabetes (T1D). This increase does not correlate with genetic drift and indicates that environmental exposures are playing an increasingly significant role. Despite major biomedical and technological advances in diagnosis and treatment, treatments are frequently insufficient as they do not inhibit the progression of the underlying autoimmune response and often fail to prevent life-threatening complications. T1D is the result of autoimmune destruction of the insulin-producing beta cells of the pancreas, and the precise, mechanistic contribution of the immune system to disease pathogenesis and progression remains to be fully characterized. Ultimately, the combinatorial effect of concurrent factors, including beta cell fragility, exogenous stressors, and genetic priming of the innate and adaptive immune system, work together to induce T1D autoimmunity. Thus, T1D is the result of immunological defects and environmental pathogens, requiring the sustained attention of collaborative research teams such as FIFE: I & D with varied perspectives, unified by the universally held goal of finding a sustainable, life-long cure. Herein, the authors provide perspective on various fields in T1D research highlighted by speakers participating in the inaugural FIFE symposium.
Highlights
Type 1 diabetes (T1D) is an autoimmune disease of unclear etiology that results in the destruction of the insulin-producing beta cells of the pancreas, causing loss of systemic blood glucose regulation and hyperglycemia, insulin resistance and chronic joint pain [1,2,3]
The event centered around immunological type 1 diabetes (T1D) research, though this minisymposium pushed beyond those boundaries by examining shared characteristics with multiple sclerosis (MS), defects in cellular metabolism, immunodeficiencies in type 2 diabetes (T2D), and the contribution of the microbiome to autoimmunity
non-obese diabetic (NOD) mice heterozygous for the melanoma differentiation-associated protein 5 (MDA5) allele and expressing roughly half as much of the receptor as WT-NOD are protected from developing T1D following CVB4 infection whereas about 50% of the WT mice become autoimmune within 7 days post-infection [19]
Summary
Type 1 diabetes (T1D) is an autoimmune disease of unclear etiology that results in the destruction of the insulin-producing beta cells of the pancreas, causing loss of systemic blood glucose regulation and hyperglycemia, insulin resistance and chronic joint pain [1,2,3]. Our lab focuses on researching the contribution of viral pathogens to T1D development and pathogenesis. Infection by picornaviruses such as coxsackievirus B (CVB) promotes T1D development through the stimulation of pancreatic inflammation, resulting in the release of islet antigens and the development of autoantigens. We aim to incorporate a perspective using models with multifactorial autoimmunity triggers by examining the contribution of gut microbiome and virome, pancreatic viral persistence, and T1Drisk genes, to determine impact on inflammation, innate sensing, and loss of regulatory mechanisms leading to onset of T1D. The event centered around immunological T1D research, though this minisymposium pushed beyond those boundaries by examining shared characteristics with multiple sclerosis (MS), defects in cellular metabolism, immunodeficiencies in type 2 diabetes (T2D), and the contribution of the microbiome to autoimmunity. A variety of approaches and experimental methods were discussed, ranging from therapeutic applications based on innovative biomaterials to translation and complementation of mouse models and clinical data for a more complete understanding of the immunological underpinnings of T1D
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