Replicative senescence of T cells is correlated with erosion of telomere ends. Telomerase plays a key role in maintaining telomere length. Therefore, it is thought that telomerase regulates the life span of T cells. To test this hypothesis, we have over-expressed human telomerase reverse transcriptase in human CD8+ T cells. Ectopic expression of human telomerase reverse transcriptase led to immortalization of these T cells, without altering the phenotype and without loss of specificity or functionality. As the T cells remained dependent on cytokines and Ag stimulation for their in vitro expansion, we conclude that immortalization was achieved without malignant transformation.

The ends of linear eukaryotic chromosomes, which are called telomeres, consist of DNA-protein complexes ending in a large duplex loop (1). They serve to maintain CHROMOSOMAL integrity and prevent end-to-end fusion of the chromosomes. Telomere length is not constant over time. The telomeric ends have a length of 5–15 kb in humans and shorten by 50–100 bp per cell division in normal somatic cells (2, 3). When telomeric ends get too short, cells will enter a state of replicative senescence followed by crisis and cell death. Thus, telomere shortening may prevent unlimited proliferation of human somatic tissues. Telomere shortening is counteracted by the RIBONUCLEOPROTEIN enzyme complex called telomerase, which has two key components, the telomerase reverse transcriptase (TERT)4 and telomerase RNA, which is used as a template to elongate telomeric ends (for reviews see Refs. 4, 5, 6). The crucial role of human (h)TERT in maintaining telomeric length and subsequently of the replicative life span of cells has been demonstrated recently. It has been documented that ectopic expression of hTERT, in cell types without endogenous expression of hTERT, led to elongation of the telomeres and to an increased life span of foreskin fibroblasts, retinal pigment epithelial cells, and endothelial cells (7, 8, 9), indicating that hTERT by itself regulates the life span of these cell types. In other cases, however, ectopic expression of hTERT was not sufficient and had to be accompanied by an inactivated Rb/p16INKa pathway to give similar effects in human mammary epithelial cells and foreskin keratinocytes (10)

A correlation between telomere shortening and life span has ALSO been found in cells of the immune system. It was reported that the average telomeric length and the replicative potential are higher in naive T cells as compared with memory T cells from the same donor, in both CD4+ cells (11, 12) and CD8+ cells (13, 14). These findings are consistent with two ex vivo studies with peripheral blood leukocytes, indicating a correlation between the loss of telomere repeat fragments and the age of the donor (15, 16). Ongoing shortening of telomeres and subsequent induction of replicative senescence in cells of the immune system occur despite the presence of endogenous hTERT in T and B cells 

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