scholarly journals Extracellular Vesicles Derived Human-miRNAs Modulate the Immune System in Type 1 Diabetes

2020 ◽  
Vol 8 ◽  
Author(s):  
Tine Tesovnik ◽  
Jernej Kovač ◽  
Katka Pohar ◽  
Samo Hudoklin ◽  
Klemen Dovč ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Extracellular Vesicles ◽  
Human Mirnas

scholarly journals Extracellular Vesicles in Immune System Regulation and Type 1 Diabetes: Cell-to-Cell Communication Mediators, Disease Biomarkers, and Promising Therapeutic Tools

2021 ◽  
Vol 12 ◽  
Author(s):  
Giuseppina Emanuela Grieco ◽  
Daniela Fignani ◽  
Caterina Formichi ◽  
Laura Nigi ◽  
Giada Licata ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Autoimmune Diseases ◽  
Extracellular Vesicles ◽  
Molecular Mechanisms ◽  
Biological Fluids ◽  
Β Cells ◽  
Pancreatic Β Cells ◽  
Disease Biomarkers

Extracellular vesicles (EVs) are generated by cells of origin through complex molecular mechanisms and released into extracellular environment. Hence, the presence of EVs has been described in multiple biological fluids and in most cases their molecular cargo, which includes non-coding RNAs (ncRNA), messenger RNAs (mRNA), and proteins, has been reported to modulate distinct biological processes. EVs release and their molecular cargo have been demonstrated to be altered in multiple diseases, including autoimmune diseases. Notably, numerous evidence showed a relevant crosstalk between immune system and interacting cells through specific EVs release. The crosstalk between insulin-producing pancreatic β cells and immune system through EVs bidirectional trafficking has yet started to be deciphered, thus uncovering an intricate communication network underlying type 1 diabetes (T1D) pathogenesis. EVs can also be found in blood plasma or serum. Indeed, the assessment of circulating EVs cargo has been shown as a promising advance in the detection of reliable biomarkers of disease progression. Of note, multiple studies showed several specific cargo alterations of EVs collected from plasma/serum of subjects affected by autoimmune diseases, including T1D subjects. In this review, we discuss the recent literature reporting evidence of EVs role in autoimmune diseases, specifically focusing on the bidirectional crosstalk between pancreatic β cells and immune system in T1D and highlight the relevant promising role of circulating EVs as disease biomarkers.

Endocrine autoimmunity

2011 ◽  
pp. 34-44 ◽  
Author(s):  
Matthew J. Simmonds ◽  
Stephen C. L. Gough
Keyword(s):  
Immune Response ◽  
Type 1 Diabetes ◽  
Immune System ◽  
Endocrine System ◽  
Graves Disease ◽  
Self Tolerance ◽  
Autoimmune Attack ◽  
Endocrine Organs

Dysfunction within the endocrine system can lead to a variety of diseases with autoimmune attack against individual components being some of the most common. Endocrine autoimmunity encompasses a spectrum of disorders including, e.g., common disorders such as type 1 diabetes, Graves’ disease, Hashimoto’s thyroiditis, and rarer disorders including Addison’s disease and the autoimmune polyendocrine syndromes type 1 (APS 1) and type 2 (APS 2) (see Table 1.6.1). Autoimmune attack within each of these diseases although aimed at different endocrine organs is caused by a breakdown in the immune system’s ability to distinguish between self and nonself antigens, leading to an immune response targeted at self tissues. Investigating the mechanisms behind this breakdown is vital to understand what has gone wrong and to determine the pathways against which therapeutics can be targeted. Before discussing how self-tolerance fails, we first have to understand how the immune system achieves self-tolerance.

scholarly journals Probiotics and Prebiotics for the Amelioration of Type 1 Diabetes: Present and Future Perspectives

2019 ◽  
Vol 7 (3) ◽  
pp. 67 ◽  
Author(s):  
Sidharth Mishra ◽  
Shaohua Wang ◽  
Ravinder Nagpal ◽  
Brandi Miller ◽  
Ria Singh ◽  
...  
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
Immune System ◽  
Gut Microbiota ◽  
Adaptive Immune Response ◽  
Early Years ◽  
Autoimmune Response ◽  
Β Cells ◽  
Environmental Interactions

Type 1-diabetes (T1D) is an autoimmune disease characterized by immune-mediated destruction of pancreatic beta (β)-cells. Genetic and environmental interactions play an important role in immune system malfunction by priming an aggressive adaptive immune response against β-cells. The microbes inhabiting the human intestine closely interact with the enteric mucosal immune system. Gut microbiota colonization and immune system maturation occur in parallel during early years of life; hence, perturbations in the gut microbiota can impair the functions of immune cells and vice-versa. Abnormal gut microbiota perturbations (dysbiosis) are often detected in T1D subjects, particularly those diagnosed as multiple-autoantibody-positive as a result of an aggressive and adverse immunoresponse. The pathogenesis of T1D involves activation of self-reactive T-cells, resulting in the destruction of β-cells by CD8+ T-lymphocytes. It is also becoming clear that gut microbes interact closely with T-cells. The amelioration of gut dysbiosis using specific probiotics and prebiotics has been found to be associated with decline in the autoimmune response (with diminished inflammation) and gut integrity (through increased expression of tight-junction proteins in the intestinal epithelium). This review discusses the potential interactions between gut microbiota and immune mechanisms that are involved in the progression of T1D and contemplates the potential effects and prospects of gut microbiota modulators, including probiotic and prebiotic interventions, in the amelioration of T1D pathology, in both human and animal models.

Modulating the immune system to delay the clinical onset of type 1 diabetes

2020 ◽  
Vol 97 (2) ◽  
pp. 248-250
Author(s):  
Mai Sugahara ◽  
Tetsuhiro Tanaka ◽  
Masaomi Nangaku
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Clinical Onset

scholarly journals The association between enteroviruses and type 1 diabetes

2012 ◽  
Vol 19 (3) ◽  
pp. 323-329
Author(s):  
Gabriela Florina Dale ◽  
Loredana Popa ◽  
Amorin Popa
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Viral Infection ◽  
Animal Studies ◽  
Human Studies ◽  
Target Tissue ◽  
Complex Interactions ◽  
Prevention And Treatment ◽  
Host Target

Abstract The hypothesis that under some circumstances enteroviral infections can lead to type1 diabetes (T1D) was proposed several decades ago, based initially on evidence fromanimal studies and sero-epidemiology. The mechanisms leading to the diseaseinvolve complex interactions between the virus, host target tissue (pancreas) and theimmune system. The following article is intended as a review of several recentinformation of the topic based on human studies that try to establish a connectionbetween a viral infection and Type 1 diabetes. Through understanding better thisassociation and it’s implications in the onset of T1D potential new ways ofprevention and treatment may emerge.

scholarly journals A roadmap of the generation of neoantigens as targets of the immune system in type 1 diabetes

2016 ◽  
Vol 43 ◽  
pp. 67-73 ◽  
Author(s):  
Bart O Roep ◽  
Maria JL Kracht ◽  
Menno van Lummel ◽  
Arnaud Zaldumbide
Keyword(s):  
Type 1 Diabetes ◽  
Immune System

scholarly journals Immune outcomes and safety of high-dose oral insulin as a primary prevention immunotherapy in young autoantibody-negative children at high genetic risk for type 1 diabetes

2020 ◽  
Author(s):  
Robin Assfalg ◽  
Jan Knoop ◽  
Kristi L. Hoffman ◽  
Markus Pfirrmann ◽  
Jose Maria Zapardiel-Gonzalo ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Immune System ◽  
Primary Prevention ◽  
Genetic Risk ◽  
Adaptive Immune System ◽  
Oral Insulin ◽  
Dependent Manner ◽  
Cell Responses ◽  
Adaptive Immune

AbstractBackgroundOral administration of antigen can induce immunological tolerance. Insulin is a key autoantigen in childhood type 1 diabetes with insulin autoimmunity often appearing in the first years of life. The aim of this study was to assess the safety and immunological effects of oral insulin immunotherapy as a primary prevention.MethodsA phase I/II randomized controlled trial (Clinicaltrials.govNCT02547519) was performed in 44 islet autoantibody-negative children aged 6 months to 2 years with familial and additional genetic risk for type 1 diabetes. Children were randomized 1:1 to daily insulin (7.5 mg with dose escalation to 67.5 mg) or placebo for 12 months. Hypoglycemia was a major safety measure. The primary immune efficacy outcome was an induction of antibody or T cell responses to oral insulin.ResultsOral insulin was well tolerated with no changes in metabolic variables. The primary immune outcome did not differ between treatment groups and responses were observed in both children who received insulin (55%) or placebo (67%). Responses were, however, modified by the type 1 diabetes INSULIN gene. Among children with a susceptible genotype, antibody responses to insulin were more frequent in insulin-treated (cumulative response, 75.8%) as compared to placebo-treated children (18.2%; P = 0.0085). Mechanistic studies identified microbiome changes that were related to INSULIN genotype and frequent treatment-independent inflammatory episodes that modified the in vitro T cell responses to insulin in children with susceptible INSULIN genotypes.ConclusionThe study demonstrated that oral insulin immunotherapy in young genetically at-risk children was safe and engaged the adaptive immune system in an INSULIN genotype-dependent manner, and linked inflammatory episodes to the activation of insulin-responsive T cells.One Sentence SummaryOral insulin given daily to very young children was safe and may engage the adaptive immune system in an INSULIN genotype-dependent manner.

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