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[Higher percentages of T regulatory cells in children at risk for developing type 1 diabetes mellitus].

Authors :
Luczyński W
Stasiak-Barmuta A
Myśliwiec M
Nikołajuk A
Brandt A
Urban R
Kos J
Juchniewicz A
Jabłońska J
Otocka A
Głowińska-Olszewska B
Florys B
Urban M
Górska M
Balcerska A
Source :
Pediatric endocrinology, diabetes, and metabolism [Pediatr Endocrinol Diabetes Metab] 2010; Vol. 16 (1), pp. 7-10.
Publication Year :
2010

Abstract

Introduction: The natural history of type 1 diabetes is concerned with the appearance of autoantibodies against antigens of pancreatic beta cells. The last decade revealed some evidence of the participation of T regulatory lymphocytes - cells which suppress immune response - in the pathogenesis of type 1 diabetes and prediabetes.<br />Aim of the Study: was the assessment of T regulatory cells in the blood of children at risk for developing type 1 the diabetes mellitus.<br />Material and Methods: 85 subjects, siblings of children with type 1 diabetes, were enrolled into the study. The presence of anti-GAD65 antibodies was assessed. With the use of flow cytometry the following cell subpopulations were noted: CD4+, CD4+CD25high and CD4+CD25highCD127low with the coexpression of: CD28, CD45RO, CD54, CD62L and CD134 molecules.<br />Results: We did not observe any differences in white blood cell count, lymphocyte (including CD4+) count and the percentage between the examined and control groups. We noted higher percentages of T regulatory cells: CD4+CD25high, CD4+CD127low and CD4+CD25highCD127low in children with the presence of anti-GAD65 antibodies as compared to the control children.<br />Conclusion: Higher percentages of T regulatory cells in the blood of children with the presence of anti-GAD65 antibodies may suggest an intensive regulatory response present in patients at risk for developing type 1 diabetes.

Details

Language :
Polish
ISSN :
2081-237X
Volume :
16
Issue :
1
Database :
MEDLINE
Journal :
Pediatric endocrinology, diabetes, and metabolism
Publication Type :
Academic Journal
Accession number :
20529599