Because TREC content is related reliably and linearly with age, measuring the TREC content in blood can be used as a tool for age determination for forensic purposes [12]. In both ESRD patients and elderly healthy individuals a decreased thymic output of naive T cells based upon TREC analysis selleck kinase inhibitor was observed. Next to the TREC content, an alternative technique to identify recent thymic emigrants is to measure the CD31 expression on naive T cells [19], which corroborates the findings of the TREC content. In addition, activation and increased numbers

of proliferating Ki-67+ naive T cells were observed. Homeostatic proliferation occurs in response to this decreased thymic output to maintain the naive T cell compartment. Our findings do not support a role for CMV in the decreased output of naive T cells or their peripheral proliferation in the periphery, as both the TREC content and the percentage of CD31+ and Ki-67+ cells were not affected by CMV serostatus. This also suggests that the expansion and differentiation of memory T cells in CMV-seropositive patients does not change the number or homeostatic proliferation of naive T cells. This may have been expected, as it is assumed that increased turnover of this compartment would also accelerate the turnover of naive T cells. Another parameter to assess the immunological age of T cells is to determine

the telomere length of CD4+ and CD8+ T cells, which is indicative of the proliferative history of the cells. Similarly to TREC content, overall there is a TGF-beta inhibitor clear inverse

correlation between RTL and age in both healthy individuals and ESRD patients. However, the CD8+ T cells of CMV-infected ESRD patients have substantially shorter telomeres than age-matched CMV-seronegative ESRD patients, resulting in an immunological age Montelukast Sodium difference of almost 20 years. This finding indicates a higher burden by CMV on CD8+ T cells of ESRD patients during ageing. We could not detect this CMV-related effect in RTL for the CD4+ T cells. The absence of additional CMV-induced telomere attrition within total CD4+ T cells in ESRD patients in contrast to that within total CD8+ T cells can therefore be explained by the difference in differentiation status of the T cell compartment. To examine whether the telomere shortage in CD8+ T cells is caused by a possible inhibitory effect on the activity of the telomerase enzyme (responsible for extending the telomere length), we analysed the activity of this enzyme in both CD8+ and CD4+ T cell populations. No differences were found between the CMV-seronegative and CMV-seropositive patients, indicating that altered telomerase activity is not a probable cause for the decreased RTL in CD8 T cells of CMV-seropositive ESRD patients. This indicates that the shorter telomeres for the CD8+ T cell compartment is caused by the higher proliferation and differentiation status in CMV-seropositive patients.