scholarly journals B-Lymphocytes Expressing an Ig Specificity Recognizing the Pancreatic β-Cell Autoantigen Peripherin Are Potent Contributors to Type 1 Diabetes Development in NOD Mice

Diabetes ◽  
2016 ◽  
Vol 65 (7) ◽  
pp. 1977-1987 ◽  
Author(s):  
Caroline M. Leeth ◽  
Jeremy Racine ◽  
Harold D. Chapman ◽  
Berta Arpa ◽  
Jorge Carrillo ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
B Lymphocytes ◽  
Nod Mice ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Diabetes Development

scholarly journals Rotavirus Infection Accelerates Type 1 Diabetes in Mice with Established Insulitis

2008 ◽  
Vol 82 (13) ◽  
pp. 6139-6149 ◽  
Author(s):  
Kate L. Graham ◽  
Natalie Sanders ◽  
Yan Tan ◽  
Janette Allison ◽  
Thomas W. H. Kay ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Nod Mice ◽  
Immune Recognition ◽  
Β Cells ◽  
Β Cell ◽  
Rotavirus Infection ◽  
Diabetes Onset ◽  
Diabetes Development

ABSTRACT Infection modulates type 1 diabetes, a common autoimmune disease characterized by the destruction of insulin-producing islet β cells in the pancreas. Childhood rotavirus infections have been associated with exacerbations in islet autoimmunity. Nonobese diabetic (NOD) mice develop lymphocytic islet infiltration (insulitis) and then clinical diabetes, whereas NOD8.3 TCR mice, transgenic for a T-cell receptor (TCR) specific for an important islet autoantigen, show more rapid diabetes onset. Oral infection of infant NOD mice with the monkey rotavirus strain RRV delays diabetes development. Here, the effect of RRV infection on diabetes development once insulitis is established was determined. NOD and NOD8.3 TCR mice were inoculated with RRV aged ≥12 and 5 weeks, respectively. Diabetes onset was significantly accelerated in both models (P < 0.024), although RRV infection was asymptomatic and confined to the intestine. The degree of diabetes acceleration was related to the serum antibody titer to RRV. RRV-infected NOD mice showed a possible trend toward increased insulitis development. Infected males showed increased CD8+ T-cell proportions in islets. Levels of β-cell major histocompatibility complex class I expression and islet tumor necrosis factor alpha mRNA were elevated in at least one model. NOD mouse exposure to mouse rotavirus in a natural experiment also accelerated diabetes. Thus, rotavirus infection after β-cell autoimmunity is established affects insulitis and exacerbates diabetes. A possible mechanism involves increased exposure of β cells to immune recognition and activation of autoreactive T cells by proinflammatory cytokines. The timing of infection relative to mouse age and degree of insulitis determines whether diabetes onset is delayed, unaltered, or accelerated.

scholarly journals A novel pancreatic β-cell targeting bispecific-antibody (BsAb) can prevent the development of Type 1 diabetes in NOD mice

2014 ◽  
Vol 153 (1) ◽  
pp. 187-198 ◽  
Author(s):  
Palash Bhattacharya ◽  
Jilao Fan ◽  
Christine Haddad ◽  
Abdul Essani ◽  
Anupama Gopisetty ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Bispecific Antibody ◽  
Nod Mice ◽  
Pancreatic Β Cell ◽  
Cell Targeting ◽  
Β Cell

scholarly journals Lymphocyte-Derived Exosomal MicroRNAs Promote Pancreatic β Cell Death and May Contribute to Type 1 Diabetes Development

2019 ◽  
Vol 29 (2) ◽  
pp. 348-361.e6 ◽  
Author(s):  
Claudiane Guay ◽  
Janine K. Kruit ◽  
Sophie Rome ◽  
Véronique Menoud ◽  
Niels L. Mulder ◽  
...  
Keyword(s):  
Cell Death ◽  
Type 1 Diabetes ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Diabetes Development

scholarly journals mt-Nd2aModifies Resistance Against Autoimmune Type 1 Diabetes in NOD Mice at the Level of the Pancreatic β-Cell

Diabetes ◽  
2010 ◽  
Vol 60 (1) ◽  
pp. 355-359 ◽  
Author(s):  
Jing Chen ◽  
Aaron M. Gusdon ◽  
Jon Piganelli ◽  
Edward H. Leiter ◽  
Clayton E. Mathews
Keyword(s):  
Type 1 Diabetes ◽  
Nod Mice ◽  
Pancreatic Β Cell ◽  
Β Cell

scholarly journals β Cell death and dysfunction during type 1 diabetes development in at-risk individuals

2015 ◽  
Vol 125 (3) ◽  
pp. 1163-1173 ◽  
Author(s):  
Kevan C. Herold ◽  
Sahar Usmani-Brown ◽  
Tara Ghazi ◽  
Jasmin Lebastchi ◽  
Craig A. Beam ◽  
...  
Keyword(s):  
At Risk ◽  
Cell Death ◽  
Type 1 Diabetes ◽  
Β Cell ◽  
Diabetes Development

scholarly journals Nonlinear Analysis for a Type-1 Diabetes Model with Focus on T-Cells and Pancreatic β-Cells Behavior

2020 ◽  
Vol 25 (2) ◽  
pp. 23
Author(s):  
Diana Gamboa ◽  
Carlos E. Vázquez ◽  
Paul J. Campos
Keyword(s):  
T Cells ◽  
Type 1 Diabetes ◽  
Cell Population ◽  
Closed Loop ◽  
Pancreatic Β Cell ◽  
Activated Macrophages ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells

Type-1 diabetes mellitus (T1DM) is an autoimmune disease that has an impact on mortality due to the destruction of insulin-producing pancreatic β -cells in the islets of Langerhans. Over the past few years, the interest in analyzing this type of disease, either in a biological or mathematical sense, has relied on the search for a treatment that guarantees full control of glucose levels. Mathematical models inspired by natural phenomena, are proposed under the prey–predator scheme. T1DM fits in this scheme due to the complicated relationship between pancreatic β -cell population growth and leukocyte population growth via the immune response. In this scenario, β -cells represent the prey, and leukocytes the predator. This paper studies the global dynamics of T1DM reported by Magombedze et al. in 2010. This model describes the interaction of resting macrophages, activated macrophages, antigen cells, autolytic T-cells, and β -cells. Therefore, the localization of compact invariant sets is applied to provide a bounded positive invariant domain in which one can ensure that once the dynamics of the T1DM enter into this domain, they will remain bounded with a maximum and minimum value. Furthermore, we analyzed this model in a closed-loop scenario based on nonlinear control theory, and proposed bases for possible control inputs, complementing the model with them. These entries are based on the existing relationship between cell–cell interaction and the role that they play in the unchaining of a diabetic condition. The closed-loop analysis aims to give a deeper understanding of the impact of autolytic T-cells and the nature of the β -cell population interaction with the innate immune system response. This analysis strengthens the proposal, providing a system free of this illness—that is, a condition wherein the pancreatic β -cell population holds and there are no antigen cells labeled by the activated macrophages.

scholarly journals Deficiency in NOD Antigen-Presenting Cell Function May Be Responsible for Suboptimal CD4+CD25+ T-Cell-Mediated Regulation and Type 1 Diabetes Development in NOD Mice

Diabetes ◽  
2006 ◽  
Vol 55 (7) ◽  
pp. 2098-2105 ◽  
Author(s):  
P. Alard ◽  
J. N. Manirarora ◽  
S. A. Parnell ◽  
J. L. Hudkins ◽  
S. L. Clark ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Cell Function ◽  
Nod Mice ◽  
Antigen Presenting Cell ◽  
Diabetes Development ◽  
Antigen Presenting

scholarly journals Spatial variations in gut permeability are linked to type 1 diabetes development in non-obese diabetic mice

2019 ◽  
Vol 7 (1) ◽  
pp. e000793
Author(s):  
William C Joesten ◽  
Audrey H Short ◽  
Michael A Kennedy
Keyword(s):  
Type 1 Diabetes ◽  
Large Intestine ◽  
Nod Mice ◽  
Spatial Variations ◽  
Gut Permeability ◽  
Spatially Resolved ◽  
Diabetes Development ◽  
End Stage ◽  
Design And Methods

ObjectivesTo determine if spatial variations in gut permeability play a role in regulating type 1 diabetes (T1D) progression.Research design and methodsSpatially resolved duodenum, jejunum, ileum, and large intestine sections from end-stage T1D non-obese diabetic (NOD) mice were probed by immunohistochemistry to quantify zonulin levels as a measure of gut permeability in early-progressor and late-progressor NOD mice in comparison with non-progressor NOD mice and healthy NOR/LtJ control mice.ResultsZonulin levels were elevated in the small and large intestines in early-progressor and late-progressor NOD mice in comparison with non-progressor NOD mice and healthy NOR control mice. In early-onset mice, elevated zonulin levels were maximum in the duodenum and jejunum and decreased in the ileum and large intestine. In late-progressor mice, zonulin levels were elevated almost evenly along the small and large intestines. In non-progressor NOD mice, zonulin levels were comparable with NOR control levels in both the small and large intestines.ConclusionsElevated zonulin expression levels indicated that gut permeability was increased both in the small and large intestines in NOD mice that progressed to end-stage T1D in comparison with non-progressor NOD mice and healthy NOR control mice. Highest elevations in zonulin levels were observed in the duodenum and jejunum followed by the ileum and large intestines. Spatial variations in gut permeability appeared to play a role in regulating the rate and severity of T1D progression in NOD mice indicating that spatial variations in gut permeability should be investigated as a potentially important factor in human T1D progression.

scholarly journals Dendritic Cell-Directed CTLA-4 Engagement during Pancreatic β Cell Antigen Presentation Delays Type 1 Diabetes

2010 ◽  
Vol 184 (12) ◽  
pp. 6695-6708 ◽  
Author(s):  
Subha Karumuthil-Melethil ◽  
Nicolas Perez ◽  
Ruobing Li ◽  
Bellur S. Prabhakar ◽  
Mark J. Holterman ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Dendritic Cell ◽  
Antigen Presentation ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Antigen

scholarly journals Manganese-Enhanced Magnetic Resonance Imaging Detects Declining Pancreatic β-Cell Mass in a Cyclophosphamide-Accelerated Mouse Model of Type 1 Diabetes

Diabetes ◽  
2012 ◽  
Vol 62 (1) ◽  
pp. 44-48 ◽  
Author(s):  
Patrick F. Antkowiak ◽  
Brian K. Stevens ◽  
Craig S. Nunemaker ◽  
Marcia McDuffie ◽  
Frederick H. Epstein
Keyword(s):  
Magnetic Resonance Imaging ◽  
Type 1 Diabetes ◽  
Magnetic Resonance ◽  
Mouse Model ◽  
Cell Mass ◽  
Pancreatic Β Cell ◽  
Resonance Imaging ◽  
Β Cell
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