A5016556462- Diabetes and associated disorders
- Pancreatic function and diabetes
- Immune Cell Function and Interaction
- Diabetes Management and Research
- Phagocytosis and Immune Regulation
- Neonatal Respiratory Health Research
- Immunotherapy and Immune Responses
- MicroRNA in disease regulation
- Child and Adolescent Health
- RNA Interference and Gene Delivery
- SARS-CoV-2 and COVID-19 Research
- Hematopoietic Stem Cell Transplantation
- Infant Nutrition and Health
Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol
2018-2025
Universitat Autònoma de Barcelona
2017-2025
Hospital Universitari Germans Trias i Pujol
2017
Based on the ability of apoptosis to induce immunological tolerance, liposomes were generated mimicking apoptotic cells, and they arrest autoimmunity in Type 1 diabetes. Our aim was validate immunotherapy other autoimmune disease: multiple sclerosis.Phosphatidylserine-rich loaded with disease-specific autoantigen. Therapeutic capability assessed vitro vivo.Liposomes induced a tolerogenic phenotype dendritic arrested autoimmunity, thus decreasing incidence, delaying onset reducing severity...
Type 1 diabetes (T1D) is a metabolic disease caused by the autoimmune destruction of insulin-producing β-cells. With its incidence increasing worldwide, to find safe approach permanently cease autoimmunity and allow β-cell recovery has become vital. Relying on inherent ability apoptotic cells induce immunological tolerance, we demonstrated that liposomes mimicking β-cells arrested prevented experimental T1D through tolerogenic dendritic cell (DC) generation. These contained...
Type 1 diabetes (T1D) results from a breakdown in immunological tolerance, with pivotal involvement of antigen-presenting cells. In this context, antigen-specific immunotherapies have been developed to arrest autoimmunity, such as phosphatidylserine (PS)-liposomes. However, the role certain cells immunotherapy, particularly human macrophages (Mφ) T1D remains elusive. The aim study was determine Mφ immune tolerance and T1D. To that end, we evaluated ability capture apoptotic-body mimicking...
Type 1 diabetes (T1D) is a chronic metabolic disease characterized by the autoimmune destruction of β-cells in pancreatic islets. T1D preceded islet-specific inflammation led several immune cells. Among them, natural killer (NK) cells are emerging as important players development. Human NK CD56 and CD16 expression, which allows classifying into four subsets: 1) dim + or effector (NK eff ); 2) bright − regulatory reg 3) intermediate cells; 4) cells, whose function not well determined. Since...
Type 1 diabetes (T1D) is an autoimmune disease caused by the destruction of insulin-producing cells. Due to ability apoptotic cells clearance induce tolerance, we previously generated liposomes rich in phophatidylserine (PS) -a feature cells- loaded with insulin peptides mimic beta-cells. PS-liposomes arrested autoimmunity experimental T1D through induction tolerance. The aim this study was investigate potential several from different autoantigens encapsulated (PS)-liposomes for prevention...
Type 1 diabetes is an autoimmune disease caused by the destruction of insulin-producing β-cells. An ideal immunotherapy should combine blockade response with recovery functional target cell mass. With aim to develop new therapies for type that could contribute β-cell mass restoration, a drug repositioning analysis based on systems biology was performed identify regenerative potential commercially available compounds. Drug strategy used identifying uses approved drugs are outside scope...
The partial remission (PR) phase, a period experienced by most patients with type 1 diabetes (T1D) soon after diagnosis, is characterized low insulin requirements and improved glycemic control. Given the great potential of this phase as therapeutic window for immunotherapies because its association immunoregulatory mechanisms β-cell protection, our objective was to find peripheral immunological biomarkers better characterization, monitoring, prediction. longitudinal follow-up 17 pediatric...
Type 1 diabetes (T1D) is prompted by defective immunological tolerance, an event in which dendritic cells (DCs) are crucial as immune response orchestrators. In fact, they contribute to maintaining tolerance self-antigens, but can also prompt immunogenic against them, leading autoimmunity. Countless factors potentially impact on the proper functionality of DCs, range from altered subset distribution, impaired phagocytic function abnormal gene expression. Moreover, T1D, metabolic...
Prenatal glucocorticoids are routinely administered to pregnant women at risk of preterm delivery in order improve survival the newborn. However, half cases, birth occurs outside beneficial period for lung development. Glucocorticoids potent immune modulators and cause apoptotic death immature T cells, we have previously shown that prenatal betamethasone treatment doses eliciting maturation induce profound thymocyte apoptosis offspring. Here, asked if there long-term consequences on...
The partial remission (PR) phase of type 1 diabetes (T1D) is an underexplored period characterized by endogenous insulin production and downmodulated autoimmunity. To comprehend the mechanisms behind this transitory develop precision medicine strategies, biomarker discovery patient stratification are unmet needs. MicroRNAs (miRNAs) small RNA molecules that negatively regulate gene expression modulate several biological processes, functioning as biomarkers for many diseases. Here, we identify...
Abstract Type 1 diabetes is an autoimmune disease caused by the destruction of insulin-producing β-cells. To revert type diabetes, suppression attack should be combined with a β-cell replacement strategy. It has been previously demonstrated that liraglutide, glucagon-like peptide-1 receptor agonist, restores mass in via α-cell transdifferentiation and neogenesis. We report here treatment liraglutide does not prevent spontaneous non-obese diabetic (NOD) mouse model, but it tends to reduce...
Abstract Non-genetic factors are crucial in the pathogenesis of type 1 diabetes (T1D), a disease caused by autoimmunity against insulin-producing β-cells. Exposure to medications prenatal period may influence immune system maturation, thus altering self-tolerance. Prenatal administration betamethasone –a synthetic glucocorticoid given women at risk preterm delivery– affect development T1D. It has been previously demonstrated that protects offspring from T1D nonobese diabetic (NOD) mice. The...
Betamethasone, a glucocorticoid used to induce lung maturation when there is risk of preterm delivery, can affect the immune system and type 1 diabetes (T1D) incidence in progeny. It has been described that prenatal betamethasone protects offspring from experimental T1D development. The main aim this study was evaluate possible association between exposure humans. Research Design Methods. A retrospective case-control with total 945 children, including 471 patients 474 healthy siblings,...
Hematopoietic stem cell (HSC) transplantation is crucial to cure hematologic malignancies. Umbilical cord blood (UCB) a source of cells, but 90% UCB units are discarded due low cellularity. Improving the engraftment capacities CD34+ cells would allow use that were so far rejected. Betamethasone induces long-term transcriptomic and epigenomic changes in immune through glucocorticoid receptor. We hypothesize could be used owing improvements induced by betamethasone. Isolated HSC from exposed...