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Loss of the balance between CD4+ Foxp3+ regulatory T cells and CD4+ IL17A+ Th17 cells in patients with type 1 diabetes

Abstract The presence of low-grade chronic inflammation is a known feature of long standing diabetes type 1. Recently, two T cell subsets, that may contribute to the disease progression are under investigation. These are Treg cells, which are specialized T cell subset, that controls the activity of...

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Published in:Human immunology 2013-06, Vol.74 (6), p.701-707
Main Authors: Ryba-Stanisławowska, Monika, Skrzypkowska, Maria, Myśliwiec, Małgorzata, Myśliwska, Jolanta
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description Abstract The presence of low-grade chronic inflammation is a known feature of long standing diabetes type 1. Recently, two T cell subsets, that may contribute to the disease progression are under investigation. These are Treg cells, which are specialized T cell subset, that controls the activity of autoreactive and inflammatory cells and Th17 cells which are involved in the pathogenesis of inflammatory and autoimmune diseases. The balance between Treg and Th17 controls inflammation and is responsible for the proper function of the immune system. An decrease of Tregs and/or increase of Th17 may induce local inflammation, which in turn may hasten the development of diabetic complications. In the present study, we have demonstrated that the Treg/Th17 balance was broken in patients with diabetes type 1 and might contribute to the progression of microvascular angiopathy.
doi_str_mv 10.1016/j.humimm.2013.01.024
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subjects Adolescent
Allergy and Immunology
Case-Control Studies
Child
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - immunology
Diabetes Mellitus, Type 1 - metabolism
Forkhead Transcription Factors - metabolism
Humans
Interleukin-17 - metabolism
Lymphocyte Count
Neovascularization, Pathologic - immunology
Neovascularization, Pathologic - metabolism
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
Th17 Cells - immunology
Th17 Cells - metabolism
Young Adult
title Loss of the balance between CD4+ Foxp3+ regulatory T cells and CD4+ IL17A+ Th17 cells in patients with type 1 diabetes
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