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Type 1 Diabetes Mouse Model

An Hla-transgenic Mouse Model Of Type 1 Diabetes That Incorporates The Reduced But Not Abolished Thymic Insulin Expression Seen In Patients

An Hla-transgenic Mouse Model Of Type 1 Diabetes That Incorporates The Reduced But Not Abolished Thymic Insulin Expression Seen In Patients

An HLA-Transgenic Mouse Model of Type 1 Diabetes That Incorporates the Reduced but Not Abolished Thymic Insulin Expression Seen in Patients 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA 2Department of Medicine, Division of Endocrinology, Albert Einstein College of Medicine, Bronx, NY 10461, USA Received 5 August 2015; Accepted 4 October 2015 Copyright 2016 Jeffrey Babad et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Type 1 diabetes (T1D) is an autoimmune disease characterized by T cell-mediated destruction of the pancreatic islet beta cells. Multiple genetic loci contribute to disease susceptibility in humans, with the most responsible locus being the major histocompatibility complex (MHC). Certain MHC alleles are predisposing, including the common HLA-A02:01. After the MHC, the locus conferring the strongest susceptibility to T1D is the regulatory region of the insulin gene, and alleles associated with reduced thymic insulin expression are predisposing. Mice express two insulin genes, Ins1 and Ins2. While both are expressed in beta cells, only Ins2 is expressed in the thymus. We have developed an HLA-A02:01-transgenic NOD-based T1D model that is heterozygous for a functional Ins2 gene. These mice exhibit reduced thymic insulin expression and accelerated disease in both genders. Immune cell populations are not grossly altered, and the mice exhibit typical signs of islet autoimmunity, including CD8 T cell responses to beta cell peptides also targeted in HLA-A02:01-positive type 1 diabetes patients. This model should find utility as a tool to Continue reading >>

Mouse Models For Type 1 Diabetes

Mouse Models For Type 1 Diabetes

See other articles in PMC that cite the published article. Our understanding of the genetics, aetiology and pathogenesis of Type 1 Diabetes (T1D) was propelled by the discovery of animal models of T1D in the late 1970s and early 1980s, particularly the non-obese diabetic (NOD) mouse. Since then, transgenic and gene-targeting technologies allowed the generation of many models with reduced genetic and pathogenic complexity. These models allowed researchers to zoom in on specific aspects of this complex disease. In this review, we provide an overview of currently available mouse models for T1D. Type I diabetes mellitus, also called juvenile diabetes or insulin-dependent diabetes, is a chronic autoimmune disorder that precipitates in genetically susceptible individuals by environmental factors. The body's own immune system attacks the -cells in the islets of Langerhans of the pancreas, destroying or damaging them sufficiently to reduce and eventually eliminate insulin production. When >8090% of the -cells have been destroyed, the production of glucagon by the neighboring -cells is de-repressed. The metabolic consequences of insulin insufficiency and glucagon excess are hyperglycemia and ketoacidosis. Type 1 diabetes is distinguished from type 2 (non-insulin-dependent) diabetes by the presence of autoantibodies, the genetic link, the insulin dependence and by insulitis, which is characterized by activated T lymphocytes. A widely used virus-induced diabetes model is the LCMV infection of RIP-GP or R/HIP-NP on the C57Bl/6, Balb/c, or NOD background. RIP-GP mice are transgenic mice expressing the lymphocytic choriomeningitis virus glycoprotein (LCMV-GP) under control of the rat insulin promoter (RIP), resulting in expression of LCMV-GP in pancreatic -cells [ 1 , 2 ]. There are Continue reading >>

Chapter 3

Chapter 3

Modified from second web edition Lang J and BellgrauD Thepast two decades has seen remarkable advances in understanding the genetics andpathophysiology of spontaneous animal models of immune mediated diabetes (Type1A) including structural characterization of class II MHC presentation of insulinpeptide B:9-23 1 as well as the chromagranin peptide WE-14 (previously elusive target ofthe BDC2.5 T cell receptor with either genetic manipulation of autoantigens 4, 5 or immunologic function (e.g.,toll receptor activation; peptide immunization, mutations of regulatorypathways such as AIRE 7), or a combination of genetic and environmental manipulation 8-18. Humanized mouse strains are being created and studied and promiseadditional insights relevant to type 1A diabetes laboratory arepository of type 1 diabetes related mouse models has been created which is animportant resource for the long-term preservation of the multiple strains thathave been created and a means to facilitate sharing of strains by differentresearch groups. Spontaneoustype 1 diabetes-susceptible models include the non-obese diabetic (NOD) mouse,the BioBreeding Diabetes-Prone (BB-DP) rat, the Komeda Diabetes-Prone (KDP)sub-line of the Long-Evans Tokushima Lean rat Lew.1.WR1 and the Lew.1AR1/Ztmrat. Multiple experimentally-induced models of type 1 diabetes are availableincluding: 1) T cell receptor (TCR) transgenic (Tg) and retrogenic mice withthe T cell receptors of naturally occurring diabetogenic clones 2) Neo-antigen(Ag) expression under the control of the rat insulin promoter (RIP) toestablish neo-self antigen pancreatic expression that can be the target ofautoimmunity, and 3) RIP-driven expression of costimulatory molecules on betacells. Mice with knockouts of putativeislet autoantigens have allowed direct Continue reading >>

Mouse Models For The Study Of Autoimmune Type 1 Diabetes: A Nod To Similarities And Differences To Human Disease

Mouse Models For The Study Of Autoimmune Type 1 Diabetes: A Nod To Similarities And Differences To Human Disease

, Volume 33, Issue1 , pp 6787 | Cite as Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease For almost 30years, the non-obese diabetic (NOD) mouse has served as the primary model for dissecting the genetic and pathogenic basis for T-lymphocyte-mediated autoimmune type 1 diabetes (T1D). However, while sharing many similarities, it is becoming increasingly appreciated that there are also some differences in the immunopathogenic basis of T1D development between humans and NOD mice. This review will focus on aspects of T1D development in NOD mice that are similar and different from that in humans. Type 1 diabetesNOD miceImmunological toleranceGenetics This article is published as part of the Special Issue on Immunopathology of the pancreas in type 1 diabetes. This is a preview of subscription content, log in to check access. Mordes JP, Serreze DV, Greiner DL, Rossini AA (2004) Animal models of autoimmune diabetes mellitus. In: LeRoith D, Taylor SI, Olefsky JM (eds) Diabetes mellitus: a fundamental and clinical text. Lippincott Williams and Wilkins, Philadelphia, pp 591610 Google Scholar Tanaguchi H, Makino S, Ikegami H (2007) The NOD mouse and its related strains. In: Shafrir E (ed) Animal models of diabetes frontiers in research, 2nd edn. CRC, Boca Raton, pp 4160 Google Scholar Delovitch TL, Singh B (1997) The nonobese diabetic mouse as a model of autoimmune diabetes: immune dysregulation gets the NOD. Immunity 7:291297 CrossRef Google Scholar Prochazka M, Leiter EH, Serreze DV, Coleman DL (1987) Three recessive loci required for insulin-dependent diabetes in NOD mice. Science 237:286289 PubMed CrossRef Google Scholar Wicker LS, Todd JA, Peterson LB (1995) Genetic control of autoimmune diabetes in the NOD mouse. Continue reading >>

Mouse Models Of Type 1 And Type 2 Diabetes Derived From The Same Closed Colony: Genetic Susceptibility Shared Between Two Types Of Diabetes

Mouse Models Of Type 1 And Type 2 Diabetes Derived From The Same Closed Colony: Genetic Susceptibility Shared Between Two Types Of Diabetes

Except for rare subtypes of diabetes, both type 1 and type 2 diabetes are multifactorial diseases in which genetic factors consisting of multiple susceptibility genes and environmental factors contribute to the disease development. Due to complex interaction among multiple susceptibility genes and between genetic and environmental factors, genetic analysis of multifactorial diseases is difficult in humans. Inbred animal models, in which the genetic background is homogeneous and environmental factors can be controlled, are therefore valuable in genetic dissection of multifactorial diseases. We are fortunate to have excellent animal models for both type 1 and type 2 diabetesthe nonobese diabetic (NOD) mouse and the Nagoya-Shibata-Yasuda (NSY) mouse, respectively. Congenic mapping of susceptibility genes for type 1 diabetes in the NOD mouse has revealed that susceptibility initially mapped as a single locus often consists of multiple components on the same chromosome, indicating the importance of congenic mapping in defining genes responsible for polygenic diseases. The NSY mouse is an inbred animal model of type 2 diabetes established from Jcl:ICR, from which the NOD mouse was also derived. We have recently mapped three major loci contributing to type 2 diabetes in the NSY mouse. Interestingly, support intervals where type 2 diabetes susceptibility genes were mapped in the NSY mouse overlapped the regions where type 1 diabetes susceptibility genes have been mapped in the NOD mouse. Although additional evidence is needed, it may be possible that some of the genes predisposing to diabetes are derived from a common ancestor contained in the original closed colony, contributing to type 1 diabetes in the NOD mouse and type 2 diabetes in the NSY mouse. Such genes, if they exis Continue reading >>

Frontiers | The Role Of Nod Mice In Type 1 Diabetes Research: Lessons From The Past And Recommendations For The Future | Endocrinology

Frontiers | The Role Of Nod Mice In Type 1 Diabetes Research: Lessons From The Past And Recommendations For The Future | Endocrinology

Front. Endocrinol., 23 February 2018 | The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future 1Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI, United States 2Department of Pathology, Immunology and Laboratory Medicine, College of Medicine, University of Florida, Gainesville, FL, United States 3Department of Animal Sciences, University of Florida, Gainesville, FL, United States For more than 35 years, the NOD mouse has been the primary animal model for studying autoimmune diabetes. During this time, striking similarities to the human disease have been uncovered. In both species, unusual polymorphisms in a major histocompatibility complex (MHC) class II molecule confer the most disease risk, disease is caused by perturbations by the same genes or different genes in the same biological pathways and that diabetes onset is preceded by the presence of circulating autoreactive T cells and autoantibodies that recognize many of the same islet antigens. However, the relevance of the NOD model is frequently challenged due to past failures translating therapies from NOD mice to humans and because the appearance of insulitis in mice and some patients is different. Nevertheless, the NOD mouse remains a pillar of autoimmune diabetes research for its usefulness as a preclinical model and because it provides access to invasive procedures as well as tissues that are rarely procured from patients or controls. The current article is focused on approaches to improve the NOD mouse by addressing reasons why immune therapies have failed to translate from mice to humans. We also propose new strategies for mixing and editing the NOD genome to improve the model in ways that will better advance our understanding of human d Continue reading >>

Variations In Rodent Models Of Type 1 Diabetes: Islet Morphology

Variations In Rodent Models Of Type 1 Diabetes: Islet Morphology

Variations in Rodent Models of Type 1 Diabetes: Islet Morphology 1Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, KS 66160, USA 2Department of Molecular Biosciences, University of Kansas, Lawrence, KS 66045, USA Received 6 February 2013; Accepted 18 April 2013 Copyright 2013 Lesya Novikova et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Type 1 diabetes (T1D) is characterized by hyperglycemia due to lost or damaged islet insulin-producing -cells. Rodent models of T1D result in hyperglycemia, but with different forms of islet deterioration. This study focused on 1 toxin-induced and 2 autoimmune rodent models of T1D: BioBreeding Diabetes Resistant rats, nonobese diabetic mice, and Dark Agouti rats treated with streptozotocin. Immunochemistry was used to evaluate the insulin levels in the -cells, cell composition, and insulitis. T1D caused complete or significant loss of -cells in all animal models, while increasing numbers of -cells. Lymphocytic infiltration was noted in and around islets early in the progression of autoimmune diabetes. The loss of lymphocytic infiltration coincided with the absence of -cells. In all models, the remaining - and -cells regrouped by relocating to the islet center. The resulting islets were smaller in size and irregularly shaped. Insulin injections subsequent to induction of toxin-induced diabetes significantly preserved -cells and islet morphology. Diabetes in animal models is anatomically heterogeneous and involves important changes in numbers and location of the remaining - and -cells. Comparisons with huma Continue reading >>

Novel Insights Into The Animal Models Of Diabetes Mellitus

Novel Insights Into The Animal Models Of Diabetes Mellitus

Novel Insights into the Animal models of Diabetes Mellitus Animal models of disease have historically played a crucial role in the investigation and explanation of disease pathophysiology and identification of drug targets. Moreover, animal models also played important role in the assessment of new drugs in vivo. Diabetes mellitus is a group of metabolic ailments, which is characterized by high blood sugar levels for a longer period. To avoid complications of disease and related economic losses and untoward concerns, prevention and early therapy are therefore necessary. Because of the inadequate usefulness of the current therapies, new therapeutic agents are required to be developed. This paper briefly reviews the animal models of type 1 and type 2 diabetes mellitus, which include natural model of diabetes, models of diabetes induced by chemicals, genetic models of diabetes, physiological model, non-obese model, surgery induced model of diabetes mellitus. Our study found that animal models played an important role in the investigation of the pathophysiology of diabetes mellitus. Also, they helped in the understanding of drug targets and testing new drugs for the mentioned disease. Additionally, a number of animal models for type 2 diabetes mellitus have been developed which also has obesity. This reflects the linkage between obesity and diabetes, a condition similar to that of the human type i.e. connection between obesity and diabetes mellitus. These animal models have abnormality in one or more genes that are connected to obesity and insulin resistance, which leads to the development of hyperglycemia [11]. There are a number of factors that affect pathogenesis of diabetes mellitus and its complications; they include obesity, insulin resistance, hyperglycemia, hyperli Continue reading >>

Type 1 Diabetes Cured In Mice Using Gene Therapy

Type 1 Diabetes Cured In Mice Using Gene Therapy

Researchers from the University of Texas Health Science Center in San Antonio have found a way to cure type 1 diabetes in mice. It is hoped that the novel technique - which boosts insulin secretion in the pancreas - will reach human clinical trials in the next 3 years. Study co-author Dr. Bruno Doiron, Ph.D., of the Division of Diabetes, and colleagues recently reported their findings in the journal Current Pharmaceutical Biotechnology. Type 1 diabetes is estimated to affect around 1.25 million children and adults in the United States. Onset of the condition is most common in childhood, but it can arise at any age. In type 1 diabetes, the immune system destroys the insulin-producing beta cells of the pancreas. Insulin is the hormone that regulates blood glucose levels. As a result, blood glucose levels become too high. There is currently no cure for type 1 diabetes; the condition is managed through diet and insulin therapy. However, in recent years, researchers have investigated replacing beta cells as a means of eradicating type 1 diabetes once and for all. Dr. Doiron and colleagues have taken a different approach with their new study. The team reveals how they used a method called gene transfer to coax other pancreatic cells into producing insulin. Using this technique, the researchers have managed to cure type 1 diabetes in mice, bringing us one step closer to curing the condition in humans. Gene transfer method led to long-term insulin secretion in mice The gene transfer technique - called Cellular Networking, Integration and Processing - involves introducing specific genes into the pancreas using a virus as a vector. The team notes that beta cells are rejected in patients with type 1 diabetes. With the gene transfer method, the newly introduced genes encourage non- Continue reading >>

The Use Of Animal Models In Diabetes Research

The Use Of Animal Models In Diabetes Research

The use of animal models in diabetes research Diabetes Research Group, King's College London, London, UK Aileen King, Diabetes Research Group, Guy's Campus, King's College London, London SE1 1UL, UK. E-mail: [email protected] Received 2011 Aug 19; Revised 2012 Feb 10; Accepted 2012 Feb 13. Copyright 2012 The Author. British Journal of Pharmacology 2012 The British Pharmacological Society This article has been cited by other articles in PMC. Diabetes is a disease characterized by a relative or absolute lack of insulin, leading to hyperglycaemia. There are two main types of diabetes: type 1 diabetes and type 2 diabetes. Type 1 diabetes is due to an autoimmune destruction of the insulin-producing pancreatic beta cells, and type 2 diabetes is caused by insulin resistance coupled by a failure of the beta cell to compensate. Animal models for type 1 diabetes range from animals with spontaneously developing autoimmune diabetes to chemical ablation of the pancreatic beta cells. Type 2 diabetes is modelled in both obese and non-obese animal models with varying degrees of insulin resistance and beta cell failure. This review outlines some of the models currently used in diabetes research. In addition, the use of transgenic and knock-out mouse models is discussed. Ideally, more than one animal model should be used to represent the diversity seen in human diabetic patients. This paper is the latest in a series of publications on the use of animal models in pharmacology research. Readers might be interested in the previous papers. Robinson V (2009). Less is more: reducing the reliance on animal models for nausea and vomiting research. Holmes AM, Rudd JA, Tattersall FD, Aziz Q, Andrews PLR (2009). Opportunities for the replacement of animals in the study of nausea and vomiting. Continue reading >>

The Use Of Animal Models In The Study Of Diabetes Mellitus

The Use Of Animal Models In The Study Of Diabetes Mellitus

Abstract Animal models have enormously contributed to the study of diabetes mellitus, a metabolic disease with abnormal glucose homeostasis, due to some defect in the secretion or the action of insulin. They give researchers the opportunity to control in vivo the genetic and environmental factors that may influence the development of the disease and establishment of its complications, and thus gain new information about its handling and treatment in humans. Most experiments are carried out on rodents, even though other species with human-like biological characteristics are also used. Animal models develop diabetes either spontaneously or by using chemical, surgical, genetic or other techniques, and depict many clinical features or related phenotypes of the disease. In this review, an overview of the most commonly used animal models of diabetes are provided, highlighting the advantages and limitations of each model, and discussing their usefulness and contribution in the field of diabetes research. Type I Diabetes (T1DM) Models T1DM, a multifactorial autoimmune disease involving genetic and environmental factors, is hallmarked by T-cell and macrophages-mediated destruction of pancreatic β-cells, resulting in irreversible insulin deficiency. Diabetic ketoacidosis, a T1DM immediate consequence, can be fatal without treatment, while the long-term vascular T1DM complications affecting several organs and tissues can significantly affect life expectancy. There is no doubt that T1DM susceptibility is MHC-dependent and MHC genes account for approximately 50% of the total contribution to the disease. However, although to date studies corroborate that both HLA-DR and HLA-DQ genes are important in determining disease risk, the effects of individual alleles may be modified by the h Continue reading >>

Lung Fibrosis In Experimental Type 1 Diabetic Mouse Model: Role Of Oxidative Stress And Inflammation

Lung Fibrosis In Experimental Type 1 Diabetic Mouse Model: Role Of Oxidative Stress And Inflammation

Lung Fibrosis in Experimental Type 1 Diabetic Mouse Model: Role of Oxidative Stress and Inflammation Diabetes impacts multiple org Diabetes impacts multiple organs to cause several life-threatening complications; however, there were limited data on the risk of pulmonary disease in patients with diabetes. A recent epidemiological study (Diabetes Care 2010) shows that individuals with diabetes are at increased risk of several pulmonary conditions (asthma, COPD, fibrosis, and pneumonia), which may be a consequence of declining lung function in patients with diabetes. However, whether the lung fibrosis in these patients is secondary to asthma or pneumonia remains an unaddressed issue. To determine whether diabetes can cause lung fibrosis without pneumonia and asthma, we used FVB mice to induce type 1 diabetes with multiple low-doses of streptozotocin (50 mg/kg daily for 5 days). Three months after diabetes onset, lungs were collected from these diabetic mice and their age-matched controls. Histological examination with H/E staining or Sirius-red staining revealed that there were significant increases in lung inflammatory responses, including massive infiltration of the inflammatory cells, pulmonary alveolar septum thickness, and small amount of exudates in alveolar space, along with a significant increase in Sirius-red staining positive materials (collagens) in diabetic lungs. To further explore the mechanisms, real time PCR and Western blotting assays showed significant increases in the plasminogen activator inhibitor-1 (PAI-1, as a both pro-inflammatory and pro-fibrotic factor), and connective tissue growth factor (CTGF, as a pivotal mediator of fibrosis), along with a significant increase in tyrosine nitration of the proteins at molecule weight from 36 to 50 kDa in the Continue reading >>

Nod Mouse

Nod Mouse

The NOD mouse is an inbred strain that originated in the Shionogi Laboratories, Fukushima, Japan as a sub-strain of the cataract-prone mouse (CTS) that was noted for its spontaneous development of hyperglycemia. It has been extensively utilized in scientific research as a polygenic model of human type 1 diabetes (T1D). NOD mice develop diabetes spontaneously between 12-30 weeks of age and share many symptomatic and pathophysiological features of T1D including; inflammation of the pancreatic islet’s of Langerhans or “insulitis”, apoptosis of insulin-producing beta cells, hyperglycemia, polyuria and weight loss eventually leading to death. The discovery of the NOD mouse in the late 1970s was a breakthrough for T1D research, and preceded the development of engineered animal models of diabetes by about 10 years. The NOD mouse has since been an invaluable tool for the study of T1D aetiology, pathogenesis and prevention. Female NOD mice experience a higher incidence (60-80%) of type 1 diabetes compared to males (10-30%) and therefore are most commonly utilized in scientific research. Studies of the autoimmune inflammatory mechanisms that precede beta cell death in NOD mice have improved scientific understanding of the pathophysiology of T1D, however their usefulness in terms of developing intervention therapies that modulate the immune system remains to be seen. Pathophysiology Overview NOD mice develop insulitis by the age of approximately 3 weeks, shortly after being weaned from their mothers. Mononuclear cell infiltrates can be found histologically within and surrounding pancreatic islets, resulting in death of beta cells. On average, 60-80% of female and 10-20% of male NOD mice will develop T1D. Female NOD mice tend to develop overt hyperglycemia indicating diabetes Continue reading >>

Validity Of Animal Models Of Type 1 Diabetes, And Strategies To Enhance Their Utility In Translational Research - Sciencedirect

Validity Of Animal Models Of Type 1 Diabetes, And Strategies To Enhance Their Utility In Translational Research - Sciencedirect

Validity of animal models of type 1 diabetes, and strategies to enhance their utility in translational research Author links open overlay panel Melanie L.Grahamab Get rights and content Type 1 diabetes currently affects 2040 million people worldwide. Insulin treatment is standard, but a majority of patients still experience glycemic instability and associated comorbidity: there is an unmet medical need for novel therapeutics. Animal models have been indispensable in testing innovative medicinal approaches since the early testing of insulin in dogs almost a century ago. Models include mainly rodents with spontaneous diabetes, or rodents and nonhuman primates in which diabetes is induced by chemicals that are toxic to insulin-producing pancreatic -cells, or by pancreatectomy. To a less extent models in pigs are used. Rodent models have shown value in studies on pathogenesis and disease prevention, while models in nonhuman primates have translational value in testing -cell replacement products and immunosuppressives to prevent rejection. Evidently, for many immunosuppressives this validation follows from the close similarity in immune function. Gene therapy approaches are being tested in both rodents and nonhuman primates. We present an overview of models used to answer various research questions, with particular focus on their translational value. This includes a consideration of divergence between the animal model and the clinical condition, and a consideration of the species and model difference in pathogenesis, especially the induction of the diabetic state. Careful attention should be given to managing diabetic animals: outcome measures in the model are highly stress-sensitive and parameters that have potential for confounding should be addressed, i.e., environment, Continue reading >>

Gene Therapy Temporarily Reverses Type 1 Diabetes In Mice

Gene Therapy Temporarily Reverses Type 1 Diabetes In Mice

Gene Therapy Temporarily Reverses Type 1 Diabetes in Mice Pancreatic cells engineered to produce insulin did not immediately provoke an immune response. Human islets were treated with a drug to kill the insulin-making cells, then treated with either an empty virus (left) or a therapeutic virus (right) and grown in a diabetic mouse. The green staining shows insulin-making cells.GEORGE GITTES AND XIANGWEI XIAOResearchers have successfully treated animals with a mouse version of type 1 diabetes by inducing pancreatic cells that dont normally produce insulin to manufacture the protein, according to a study published today (January 4) in Cell Stem Cell . The research team, based at the University of Pittsburgh School of Medicine, didnt expect the experiment to worksince type 1 diabetes arises when the immune system turns on cells that naturally produce insulin, they expected that inflammation would quickly wipe out the engineered cells as well. But instead, the mice thrived for four months before an immune reaction destroyed the cells. Type 1 diabetes is an autoimmune disease where the body is reacting to the insulin-producing cells and killing them off and we dont really know why, study coauthor George Gittes, a physician scientist at the Childrens Hospital of Pittsburgh, tells Gizmodo . If you gave patients new insulin cells with a transplant, it will kill them off. If we use gene therapy to get the body to make new insulin-producing cells in the body, logically it should attack those cells too. Gittes and his colleagues constructed an adeno-associated virus to carry genetic material that would direct so-called alpha cells in the pancreas to produce insulinnormally the job of beta cells. They then delivered the virus directly to the pancreas of mouse models of type 1 diab Continue reading >>

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