SULM – Schweizerische Union für Labormedizin | Union Suisse de Médecine de Laboratoire | Swiss Union of Laboratory Medicine

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B Brando1 , A Longo1 , B Beltrami2 , D Passoni2 , R Verna3 , F Licastro4 , M Corsi2

1Lab of Transplant Immunology and Hematologic Diagnosis, Hospital Niguarda, Milan, Italy, 2Institute of General Pathology, Lab of Clinical Pathology, University of Milan, Italy, 3Dept of Experimental Medicine and Pathology, Clinical Pathology, University La Sapienza, Rome, Italy, 4Dept of Experimental Pathology, Section of Immunology, University of Bologna, Italy

The decline of immune cell function during aging suggests that these cells might be a good model to explore the role of the in vivo replicative senescence during aging. Telomere shortening may play a role in cellular aging, and one might be able to predict critically shortened telomeres in the lymphocytes in age associated diseases. We wanted to see whether increased telomere length is associated with the premature immunosenescence of lymphocytes in individuals with Down syndrome. To investigate the effects of aging and trisomy 21 on telomere length in vivo, we employed a new method based on flow-FISH, the DAKO Telomere PNA kit/FITC (DakoCytomation, Milan, Italy), never used before in these patients. We obtained 19 Down syndrome individuals (age 18-60 years) divided into three groups: group A < 30 years, group B between 30 and 50 years, and group C >50 years. Telomere length (RTL) was determined by fluorescence in situ hybridization and flow cytometry analysis. Telomere fluorescence was acquired on a FACSCalibur (Becton Dickinson). We set the gates of our cytometer around the G0/1 phase for PBMC and control cells (1301 line) on the basis of DNA content. We found an age-related telomere loss in Down syndrome patients, as previously described elsewhere. There was a significant loss of telomere length between group A (23.87 + 6.73 SD) and B (13.36 + 4.21 SD) (p < 0.01) and between group A (23.87 + 6.73 SD) and C ( 11.18 + 3.92 SD)(p < 0.001). These findings that telomeres in PBMCs from Down syndrome patients become shorter during aging in vivo support the suggestion that this loss may be involved in replicative senescence.


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