Regulatory T cells with CD62L or TNFR2 expression in young type 1 diabetic patients: relation to inflammation, glycemic control and micro-vascular complications

2015 ◽  
Vol 29 (1) ◽  
pp. 120-126 ◽  
Author(s):  
Mona H. El-Samahy ◽  
Amira A.M. Adly ◽  
Eman A. Ismail ◽  
Nouran Yousef Salah
Endocrine ◽  
2009 ◽  
Vol 35 (3) ◽  
pp. 420-428 ◽  
Author(s):  
Núria Alonso ◽  
María Jesús Martínez-Arconada ◽  
María Luisa Granada ◽  
Berta Soldevila ◽  
Ana Cantón ◽  
...  

2006 ◽  
Vol 177 (12) ◽  
pp. 8338-8347 ◽  
Author(s):  
Manuela Battaglia ◽  
Angela Stabilini ◽  
Barbara Migliavacca ◽  
Jutta Horejs-Hoeck ◽  
Thomas Kaupper ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Monika Ryba ◽  
Karolina Rybarczyk-Kapturska ◽  
Katarzyna Zorena ◽  
Małgorzata Myśliwiec ◽  
Jolanta Myśliwska

Diabetes type 1 is a chronic autoimmune disease in which insulin-producing cells are gradually destroyed by autoreactive T cells. Human regulatory cells play important role in controlling autoimmunity, and their qualitative or quantitative dysfunctions may result in ineffective suppression of autoreactive T cells. CD62L is a surface molecule that plays role in homing capabilities of Tregs, and only cells with high expression of CD62L have high suppressive potential. Tregs are also characterized by the constant expression of TNFR2. The frequency of Tregs carrying TNFR2 is higher in inflammatory conditions. We investigated blood regulatory T cells with CD62L expression and regulatory T cells expressing TNFR2 in type 1 diabetic patients. We found differences in these populations when comparing to healthy individuals. We propose that these may be associated with inflammatory conditions that are present in patients with type 1 diabetes. The lower percentage of Tregs and Treg CD62Lhighmay contribute to ineffective suppression of proinflammatory cytokines production during type 1 diabetes.


Endocrine ◽  
2013 ◽  
Vol 46 (2) ◽  
pp. 256-262 ◽  
Author(s):  
Maria Ida Maiorino ◽  
Giuseppe Bellastella ◽  
Michela Petrizzo ◽  
Maria Rosaria Improta ◽  
Clementina Brancario ◽  
...  

2006 ◽  
Vol 154 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Lars Melholt Rasmussen ◽  
Lise Tarnow ◽  
Troels Krarup Hansen ◽  
Hans-Henrik Parving ◽  
Allan Flyvbjerg

Objective: The bone-related peptide osteoprotegerin (OPG) has recently been found in increased amounts in the vasculature in diabetes. It is produced by vascular smooth muscle and endothelial cells, and may be implicated in the development of vascular calcifications. OPG is present in the circulation, where increased amounts have been observed in patients with diabetes. In this study, we examined whether plasma OPG is associated with the glycaemic and vascular status of patients with type 1 diabetes. Methods: Two gender-, age- and duration-comparable groups of type 1 diabetic patients either with (n = 199) or without (n = 192) signs of diabetic nephropathy were studied. Plasma OPG was determined by an ELISA. Results: The plasma OPG concentration was significantly higher in patients with nephropathy than those without (3.11 (2.49–3.99) vs 2.57 (2.19–3.21) (median (interquartiles), ng/ml), P < 0.001). Plasma OPG correlated with haemoglobin A1c (HbA1c), systolic blood pressure and age in both groups and, in addition, with kidney function in the nephropathic group. These correlations remained significant in multivariate models. In addition, we found that plasma OPG concentrations were increased among patients with cardiovascular diseases (CVD), both in the normoalbuminuric and the nephropathic groups. The differences between nephropathic and normoalbuminuric, as well as subgroups with and without CVD, could largely be ascribed to changes in HbA1c, age, systolic blood pressure and creatinine. Conclusion: OPG is associated with glycaemic control and CVD in patients with type 1 diabetes, compatible with the hypothesis that OPG is associated with the development of diabetic vascular complications.


2006 ◽  
Vol 4 (3) ◽  
pp. 686-688 ◽  
Author(s):  
I. SELJEFLOT ◽  
J. R. LARSEN ◽  
K. DAHL-JORGENSEN ◽  
K. F. HANSSEN ◽  
H. ARNESEN

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