scholarly journals Analysis of the autoimmune regulator (Aire)-dependent transcriptome in thymic medullary epithelial cells (MEC) and pancreatic islet β cells from non-obese diabetic (NOD) mice

2019 ◽  
Author(s):  
M Guerau-de-Arellano
Keyword(s):  
Epithelial Cells ◽  
Pancreatic Islet ◽  
Nod Mice ◽  
Β Cells ◽  
Autoimmune Regulator ◽  
Medullary Epithelial Cells

scholarly journals Aire controls the expression of Prss29 in the thymus.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Epithelial Cells ◽  
Negative Selection ◽  
Wild Type ◽  
Knock Out ◽  
Autoimmune Regulator ◽  
Specific Protease ◽  
Knock Out Mice ◽  
Medullary Epithelial Cells

Aire, the autoimmune regulator, promotes promiscuous transcription of tissue-restricted antigen in the thymus for negative selection (1, 2). By studying the transcriptomes of the thymuses of Aire knock-out mice using two independent published datasets (3, 4), we found that Prss29 was among the genes whose expression most changes between wild-type and Aire knock-out mice in the medullary epithelial cells of the thymus. The expression of Prss29 was significantly decreased in the absence of Aire. Prss29 is an implantation-specific protease that is important for the processes of embryonic invasion and implantation (5). We conclude that Aire controls the expression of Prss29 in the thymus and suggest that this may function in immunological privilege of the fetus.

Electron microscope study of the secretory activity of epithelial cells in embryonic thymus

1990 ◽  
Vol 48 (3) ◽  
pp. 382-383
Author(s):  
H. Alasam
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Epithelial Cells ◽  
Electron Density ◽  
Secretory Activity ◽  
T Cell Differentiation ◽  
High Electron ◽  
Transmission Electron ◽  
Medullary Epithelial Cells ◽  
Thymic Factor

The possibility that intrathymic T-cell differentiation involves stem cell-lymphoid interactions in embryos led us to study the ultrastructure of epithelial cell in normal embryonic thymus. Studies in adult thymus showed that it produces several peptides that induce T-cell differentiation. Several of them have been chemically characterized, such as thymosin α 1, thymopoietin, thymic humoral factor or the serum thymic factor. It was suggested that most of these factors are secreted by populations of A and B-epithelial cells.Embryonic materials were obtained from inbred matings of Swiss Albino mice. Thymuses were disected from embryos 17 days old and prepared for transmission electron microscopy. Our studies showed that embryonic thymus at this stage contains undifferentiated and differentiated epithelial cells, large lymphoblasts, medium and few small lymphocytes (Fig. 5). No differences were found between cortical and medullary epithelial cells, in contrast to the findings of Van Vliet et al,. Epithelial cells were mostly of the A-type with low electron density in both cytoplasm and nucleus. However few B-type with high electron density were also found (Fig. 7).

scholarly journals Lymphotoxin Pathway and Aire Influences on Thymic Medullary Epithelial Cells Are Unconnected

2007 ◽  
Vol 179 (9) ◽  
pp. 5693-5700 ◽  
Author(s):  
Emily S. Venanzi ◽  
Daniel H. D. Gray ◽  
Christophe Benoist ◽  
Diane Mathis
Keyword(s):  
Epithelial Cells ◽  
Medullary Epithelial Cells

scholarly journals Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase

2003 ◽  
Vol 197 (12) ◽  
pp. 1635-1644 ◽  
Author(s):  
Elmar Jaeckel ◽  
Ludger Klein ◽  
Natalia Martin-Orozco ◽  
Harald von Boehmer
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Tolerance Induction ◽  
Nod Mice ◽  
Normal Incidence ◽  
Invariant Chain ◽  
Acid Decarboxylase ◽  
Β Cells ◽  
Nonobese Diabetic ◽  
Specific Tolerance

Experiments in nonobese diabetic (NOD) mice that lacked expression of glutamic acid decarboxylase (GAD) in β cells have suggested that GAD represents an autoantigen essential for initiating and maintaining the diabetogenic immune response. Several attempts of inducing GAD-specific recessive tolerance to support this hypothesis have failed. Here we report on successful tolerance induction by expressing a modified form of GAD under control of the invariant chain promoter resulting in efficient epitope display. In spite of specific tolerance insulitis and diabetes occurred with normal kinetics indicating that GAD is not an essential autoantigen in the pathogenesis of diabetes.

scholarly journals An AP-3-dependent mechanism drives synaptic-like microvesicle biogenesis in pancreatic islet β-cells

2010 ◽  
Vol 299 (1) ◽  
pp. E23-E32 ◽  
Author(s):  
Arthur T. Suckow ◽  
Branch Craige ◽  
Victor Faundez ◽  
William J. Cain ◽  
Steven D. Chessler
Keyword(s):  
Synaptic Vesicle ◽  
Pancreatic Islet ◽  
Membrane Trafficking ◽  
Protein Complexes ◽  
Brefeldin A ◽  
Adaptor Protein ◽  
Β Cells ◽  
Β Cell ◽  
Subunit Expression ◽  
Bona Fide

Pancreatic islet β-cells contain synaptic-like microvesicles (SLMVs). The origin, trafficking, and role of these SLMVs are poorly understood. In neurons, synaptic vesicle (SV) biogenesis is mediated by two different cytosolic adaptor protein complexes, a ubiquitous AP-2 complex and the neuron-specific AP-3B complex. Mice lacking AP-3B subunits exhibit impaired GABAergic (inhibitory) neurotransmission and reduced neuronal vesicular GABA transporter (VGAT) content. Since β-cell maturation and exocytotic function seem to parallel that of the inhibitory synapse, we predicted that AP-3B-associated vesicles would be present in β-cells. Here, we test the hypothesis that AP-3B is expressed in islets and mediates β-cell SLMV biogenesis. A secondary aim was to test whether the sedimentation properties of INS-1 β-cell microvesicles are identical to those of bona fide SLMVs isolated from PC12 cells. Our results show that the two neuron-specific AP-3 subunits β3B and μ3B are expressed in β-cells, the first time these proteins have been found to be expressed outside the nervous system. We found that β-cell SLMVs share the same sedimentation properties as PC12 SLMVs and contain SV proteins that sort specifically to AP-3B-associated vesicles in the brain. Brefeldin A, a drug that interferes with AP-3-mediated SV biogenesis, inhibits the delivery of AP-3 cargoes to β-cell SLMVs. Consistent with a role for AP-3 in the biogenesis of GABAergic SLMV in β-cells, INS-1 cell VGAT content decreases upon inhibition of AP-3 δ-subunit expression. Our findings suggest that β-cells and neurons share molecules and mechanisms important for mediating the neuron-specific membrane trafficking pathways that underlie synaptic vesicle formation.

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