Estela Rosell‐Mases

ORCID: 0000-0001-6168-5937
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About
Contact & Profiles
Research Areas
  • Diabetes and associated disorders
  • Diabetes Management and Research
  • Immune Cell Function and Interaction
  • Gut microbiota and health
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Pain Mechanisms and Treatments
  • Hereditary Neurological Disorders
  • Pancreatic function and diabetes
  • Endoplasmic Reticulum Stress and Disease
  • Phagocytosis and Immune Regulation

Biomedical Research Institute of Lleida
2015-2023

Universitat de Lleida
2015-2023

Autoimmune diseases (AIDs) are caused by the loss of self-tolerance and destruction tissues host's immune system. Several antigen-specific immunotherapies, focused on arresting autoimmune attack, have been tested in clinical trials with discouraging results. Therefore, there is a need for innovative strategies to restore safely definitively AIDs. We previously demonstrated therapeutic efficacy phosphatidylserine (PS)-liposomes encapsulating autoantigens experimental type 1 diabetes multiple...

10.1016/j.nano.2022.102635 article EN cc-by-nc-nd Nanomedicine Nanotechnology Biology and Medicine 2022-12-06

Although the autoimmune destruction of pancreatic β-cells underlying type 1 diabetes (T1D) development is ultimately mediated by T cells in NOD mice and also likely humans, B play an additional key pathogenic role. It appears that expression plasma membrane–bound Ig molecules efficiently capture β-cell antigens allows autoreactive bypass normal tolerance induction processes to be subset antigen-presenting most activating diabetogenic cells. transgenically expressing recognizing are (insulin)...

10.2337/db15-1606 article EN Diabetes 2016-03-09

Autoreactive B lymphocytes play a key role as APCs in diaebetogenesis. However, it remains unclear whether B‐cell tolerance is compromised NOD mice. Here, we describe new lymphocyte transgenic mouse model, the 116C‐NOD mouse, where transgenes derive from an islet‐infiltrating of (8.3‐NODxNOR) F1 mouse. The produces clonal with pancreatic islet beta cell specificity. incidence T1D mice decreased both genders when compared Moreover, several immune selection mechanisms (including deletion and...

10.1002/eji.201445376 article EN European Journal of Immunology 2015-12-08

Previous studies indicate that B-lymphocytes play a key role activating diabetogenic T-lymphocytes during the development of autoimmune diabetes .Recently, two transgenic NOD mouse models were generated: NOD-PerIg and 116C-NOD mice. In mice, acquire an activated proliferative phenotype support accelerated development. contrast, in display anergic-like delaying onset decreasing disease incidence. The present study further evaluates T- B-lymphocyte both models. islet-infiltrating (IIBLs) from...

10.3389/fimmu.2019.01732 article EN cc-by Frontiers in Immunology 2019-07-25

Abstract Objective Type 1 diabetes (T1D) has been associated with alterations of the gut microbiota. Here we investigate cross-talk between immune system and intestinal microbiota in murine T1D. Design To evaluate modulation T1D by microbiota, non-obese diabetic (NOD) mice were cohoused 116C-NOD B-cell transgenic model. further explore influence adaptive NOD models on their fecal studied immunodeficient variants NOD.RAG-2 -/- 116C-NOD.RAG-2 , as well a non-T1D-prone mouse control. The role B...

10.21203/rs.3.rs-2512837/v1 preprint EN cc-by Research Square (Research Square) 2023-02-07

Introduction During the development of Autoimmune Diabetes (AD) an autoimmune attack against Peripheral Nervous System occurs. To gain insight into this topic, analyses Dorsal Root Ganglia (DRG) from Non-Obese Diabetic (NOD) mice were carried out. Methods Histopathological analysis by electron and optical microscopy in DRG samples, mRNA expression analyzes microarray technique blood leukocyte samples NOD C57BL/6 performed. Results The results showed formation cytoplasmic vacuoles cells early...

10.3389/fendo.2023.1176566 article EN cc-by Frontiers in Endocrinology 2023-06-02
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