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Psychosocial Factors and Telomere Length in Peripheral Blood

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Immunosenescence

Abstract

Telomeres are repetitive DNA sequences that, together with protein complexes, cap and protect eukaryotic chromosomes (Blackburn, FEBS Lett 579:859–862, 2005b). Telomeres are shortened when cells undergo mitosis due to the inability of DNA polymerase to fully extend chromosome ends during cell division (Von Zglinicki, Exp Gerontol 38:1259–1264, 2003). Telomeres prevent the ends of the chromosomes from being recognized as a double stranded DNA break, potentially triggering cell cycle arrest (Jain and Cooper, Annu Rev Genet 44:243–269, 2010). Critically short telomeres can lead to cellular senescence, when replication is no longer possible, and genomic instability, for example when chromosomes fuse end to end (Blackburn, Mol Cancer Res 3:477–482, 2005a; Shay and Wright, Carcinogenesis 26:867–874, 2005). Loss of telomere length (TL) can be countered by the enzyme telomerase, which extends TL by adding DNA sequence repeats to the ends of the chromosomes, a process that is carefully regulated throughout the lifespan of the organism (Bekaert et al., Dev Biol 274:15–30, 2004; Hathcock et al., Immunol Rev 205:104–113, 2005). Although telomerase expression is absent or low in most adult somatic cells, its expression in lymphocytes is necessary for the extensive rounds of cell division that characterize the adaptive immune response (Weng et al., Immunity 9:151–157, 1998). Telomerase expression also helps maintain stem cell function in rapidly dividing tissues, including hematopoetic stem cells and precursors (Lansdorp, Ann N Y Acad Sci 1044:220–227, 2005).

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Correspondence to Christine G. Parks .

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Parks, C.G., DeRoo, L.A. (2013). Psychosocial Factors and Telomere Length in Peripheral Blood. In: Bosch, J., Phillips, A., Lord, J. (eds) Immunosenescence. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-4776-4_7

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