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- Title
Podwyższone odsetki limfocytów T regulatorowych u dzieci z grupy ryzyka zachorowania na cukrzycę typu 1.
- Authors
ŀuczyński, Wtodzimierz; Stasiak-Barmuta, Anna; Myūliwiec, MaŁgorzata; Nikotajuk, Agnieszka; Brandt, Agnieszka; Urban, Remigiusz; Kos, Justyna; Juchniewicz, Agnieszka; JabŁońska, Jolanta; Otocka, Agnieszka; Gtowińska-Olszewska, Barbara; Florys, Bozena; Urban, Mirosńawa; Górska, Maria; Balcerska, Anna
- 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. 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. 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+CD25 high and CD4+CD25 high CD127 low with the coexpression of: CD28, CD45RO, CD54, CD62L and CD134 molecules. 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+CD25 high, CO4+CD1271ow and CD4+CD25 high CD127 low in children with the presence of anti-GAD65 antibodies as compared to the control children. 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.
- Subjects
T cells; DIABETES in children; AUTOANTIBODIES; ANTIGENS; PANCREATIC beta cells; LYMPHOCYTES
- Publication
Pediatric Endocrinology, Diabetes & Metabolism, 2010, Vol 16, Issue 1, p7
- ISSN
2083-8441
- Publication type
Article