Direct ex vivo Enumeration of CD8 T Cells Specific for β-cell Autoantigens by Peptide-HLA Multimers in Type 1 Diabetes

2010 ◽  
Vol 135 ◽  
pp. S21
Author(s):  
Anna Skowera ◽  
Sefina Arif ◽  
Anna Zaremba ◽  
Colin Dayan ◽  
Bart Roep ◽  
...  
2019 ◽  
Vol 199 (3) ◽  
pp. 263-277 ◽  
Author(s):  
L. Yeo ◽  
I. Pujol‐Autonell ◽  
R. Baptista ◽  
M. Eichmann ◽  
D. Kronenberg‐Versteeg ◽  
...  

2007 ◽  
Vol 123 ◽  
pp. S10
Author(s):  
Anna Skowera ◽  
Richard Ellis ◽  
Timothy Tree ◽  
Mark Peakman ◽  
Sefina Arif
Keyword(s):  
T Cells ◽  

2017 ◽  
Vol 65 (4) ◽  
pp. 275-284 ◽  
Author(s):  
Rubén Varela-Calvino ◽  
Cristina Calviño-Sampedro ◽  
Iria Gómez-Touriño ◽  
Oscar J. Cordero
Keyword(s):  
T Cells ◽  

2021 ◽  
pp. ji2100362
Author(s):  
Ashley E. Ciecko ◽  
David M. Schauder ◽  
Bardees Foda ◽  
Galina Petrova ◽  
Moujtaba Y. Kasmani ◽  
...  
Keyword(s):  
T Cells ◽  

2021 ◽  
pp. 108893
Author(s):  
Daisuke Chujo ◽  
Akitsu Kawabe ◽  
Maya Matsushita ◽  
Chiharu Tsutsumi ◽  
Fumitaka Haseda ◽  
...  

2020 ◽  
Vol 25 (2) ◽  
pp. 23
Author(s):  
Diana Gamboa ◽  
Carlos E. Vázquez ◽  
Paul J. Campos

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.


2019 ◽  
Vol 104 (10) ◽  
pp. 4282-4294 ◽  
Author(s):  
Mikako Takita ◽  
Erika Jimbo ◽  
Tomoyasu Fukui ◽  
Kaoru Aida ◽  
Akira Shimada ◽  
...  

Abstract Context There are scant reports on the pathological changes of the exocrine and endocrine pancreas in fulminant type 1 diabetes mellitus (FT1DM). Objective To clarify the distinct pathological changes in the exocrine as well as the endocrine pancreas shortly after onset of diabetes in FT1DM. Design The exocrine and endocrine pancreases of 3 patients with FT1DM and 17 nondiabetic controls were immunohistochemically examined for islet and exocrine tissue inflammation, infiltrating mononuclear cell (MNC) CD subtype, enterovirus capsid protein 1 (VP1) localization, and CXC chemokine ligand 10 (CXCL10) and CXC chemokine receptor 3 (CXCR3) expressions. Results The median frequency of insulitis in the 3 FT1DM pancreases was 60%. In the nondiabetic control pancreases, no insulitis was observed. In the islets of FT1DM, the numbers of CD45+, CD3+, CD8+, CD68+, and CD11c+ MNCs were significantly higher than those of the control group. In the exocrine pancreas of FT1DM, the numbers of CD3+ T cells, CD8+ T cells, CD68+ macrophages, and CD11c+ dendritic cells were significantly higher than those of the control group. Infiltrating CD8+ T cells, CD68+ macrophages, and CD11c+ dendritic cells were observed around exocrine acinar cells in FT1DM. There was a close association between VP1 and CXCL10 expression in pancreatic exocrine ductal cells and acinar cells as well as islet cells in FT1DM. CXCL10+ exocrine cells were surrounded by CXCR3+ T cells. Conclusion The pathological findings suggested that suppression of the activated CXCL10–CXCR3 axis in the exocrine as well as the endocrine pancreas is a novel therapeutic target in FT1DM and possibly in enterovirus-associated acute-onset type 1 diabetes.


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