Type 1 diabetes is driven by T-cell autoimmunity to pancreatic islet cells.
AUTOIMMUNITY
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UK researchers find equal distribution of autoimmune-mediated diabetes below and above age 30 years, but after 30 this is "spotting a needle in a haystack," as cases are far exceeded by type 2 diabetes. 
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Diabetologia. 2016 Sep 3. [Epub ahead of print]
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Cytotoxic T lymphocytes execute the killing of insulin-producing beta cells during onset of type 1 diabetes mellitus (T1D). The research community has come far in dissecting the major events in the development of this disease, but still the trigger and high-resolved information of the immunological events leading up to beta cell loss are missing. During the past decades, intravital imaging of immune responses has led to significant scientific breakthroughs in diverse models of disease, including T1D. Dynamic imaging of immune cells at the pancreatic islets during T1D onset has been made possible through the development of both advanced microscopes, and animal models that allow long-term immobilization of the pancreas. The use of these modalities has revealed a milling microenvironment at the pancreatic islets during disease onset with a plethora of active players. Clues to answering the remaining questions in this disease may lie in intravital imaging, including how key immune cells traffic to and from the pancreas, and how cells interact at this target tissue. This review highlights and discusses recent studies, models, and techniques focused to understand the immune responses during T1D onset through intravital imaging.
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The latest approach to islet transplantation, in which clusters of insulin-producing cells known as islets are transplanted from a donor pancreas into another person’s liver, has produced substantially improved results for patients with type...
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OBJECTIVE β-Cell autoantibodies are a feature of the preclinical phase of type 1 diabetes. Here, we asked how frequently they revert in a cohort of children at risk for type 1 diabetes and whether reversion has any effect on type 1 diabetes risk.
Remi Creusot's curator insight,
June 21, 2016 7:44 PM
Conversion is when a subject acquire an autoantibody, reversion is when an antibody disappears. This study looked at what it mean for a subject to "revert" and whether it reduces the risk of T1D. The study showed that the risk of having type 1 diabetes was 1.8 and 0.14 per person-years among children who remained single-autoantibody positive and those who reverted from single autoantibodies to autoantibody negative, respectively, compared with 0.06 among children who never developed autoantibodies. Researchers examined the frequency of beta cell autoantibody reversion in children at risk for type 1 diabetes, aged up to 10, and found that reversion for autoantibodies to GAD65 and insulin was 19% and 29%, respectively, and generally seen among those with single autoantibodies.
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Scientists at the UC Davis MIND Institute report that mothers of children with autism and were diagnosed with metabolic conditions during pregnancy, particularly gestational and type 2 diabetes, were more likely to have anti-fetal brain autoantibodies in their blood compared to healthy women of children with autism.
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Progress and challenges for treating Type 1 diabetes
Gilbert C FAURE's insight:
Paper Order Journal View Articles Highlighted article – May 2016 Progress and challenges for treating Type 1 diabetes Justin W. Garyua, Eric Meffrea, Chris Cotsapasc, Kevan C. Herold Journal of Autoimmunity, Available online 17 May 2016 Full article on Science Direct - free access until 26 November 2016
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This is an interview with Gary Harlem, CEO of Altucell, a company exploring novel cell therapy approaches to treating Type I diabetes.
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Aim: To evaluate the temporal trend and extent of screening for celiac disease in an Italian pediatric population of incident type 1 diabetes in the period 2006–2011, providing information on adherence to guidelines in primary care.
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One year after the introduction of the Bavarian pilot project Fr1da, medical researchers have published the first results.
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Some forms of bacteria may cause killer T cells to destroy insulin-producing beta cells in the pancreas, leading to type 1 diabetes, a new study suggests.
Gilbert C FAURE's insight:
JCI
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Gilbert C FAURE's insight:
classical but documented
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This study aimed to determine the frequency of residual beta cell function in individuals with long-standing type 1 diabetes who were recruited at diagnosis, and relate this to baseline and current is...
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Sci Rep. 2016 Sep 8;6:32899. doi: 10.1038/srep32899.
Gilbert C FAURE's insight:
Diabètes
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Autoimmunity Markers in Patients with Type 2 Diabetes, Journal of Clinical Diabetes & Practice.
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Research from JAMA — Omega-3 Polyunsaturated Fatty Acid Intake and Islet Autoimmunity in Children at Increased Risk for Type 1 Diabetes — ContextCod liver oil supplements in infancy have been associated with a decreased risk of type 1...
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An ongoing study into the understanding how and why type 1 diabetes develops has uncovered changes in the risk of type 1 diabetes related to autoantibody status.
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Type 1 diabetes (T1D) is an autoimmune disease that is triggered by both genetic and environmental factors, resulting in the destruction of pancreatic β cells. The disruption of the intestinal epithelial barrier and consequent escape of microbial products may be one of these environmental triggers. However, the immune receptors that are activated in this context remain elusive. We show here that during streptozotocin (STZ)-induced T1D, the nucleotide-binding oligomerization domain containing 2 (NOD2), but not NOD1, participates in the pathogenesis of the disease by inducing T helper 1 (Th1) and Th17 cells in the pancreatic LNs (PLNs) and pancreas. Additionally, STZ-injected wild-type (WT) diabetic mice displayed an altered gut microbiota compared with vehicle-injected WT mice, together with the translocation of bacteria to the PLNs. Interestingly, WT mice treated with broad-spectrum antibiotics (Abx) were fully protected from STZ-induced T1D, which correlated with the abrogation of bacterial translocation to the PLNs. Notably, when Abx-treated STZ-injected WT mice received the NOD2 ligand muramyl dipeptide, both hyperglycemia and the proinflammatory immune response were restored. Our results demonstrate that the recognition of bacterial products by NOD2 inside the PLNs contributes to T1D development, establishing a new putative target for intervention during the early stages of the disease.
Gilbert C FAURE's insight:
in mice
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Autoimmune diseases (AID) as a whole represent a major health concern, and remain a medical and scientific challenge. Some of them such as multiple sclerosis or type 1 diabetes have been actively investigated for many decades. Autoimmune myopathies (AIM), also referred to as idiopathic inflammatory myopathies or myositis, represent a group of very severe AID for which we have a more limited pathophysiological knowledge. AIM encompass a group of individually rare but collectively not so uncommon diseases characterized by symmetrical proximal muscle weakness, increased serum muscle enzymes such as creatine kinase, myopathic changes on electromyography and several typical histological patterns on muscle biopsy, including the presence of inflammatory cell infiltrates in muscle tissue. Importantly, some AIMs are strongly related to cancer. Here, we reviewed the current knowledge on the most prevalent forms of AIM and, notably, the diagnostic contribution of auto-antibodies (aAbs).
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Over-the-counter tests have made it easy to screen yourself for serious illnesses such as cancer and diabetes. But there are no cures for most hereditary conditions
Gilbert C FAURE's insight:
type I autoimmune diabetes
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Blocking the activation of T cells in response to proinsulin could help quell the autoimmune attack in the pancreas.
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From @BMJ_Open - Capillary blood islet autoantibody screening for identifying pre-T1D in the general population - https://t.co/RiuNkl3fom
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Researchers have made a discovery regarding the cause of Type 1 diabetes.
Gilbert C FAURE's insight:
bis
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