BackgroundAging affects the immune system and elderly people are more susceptible to diseases caused by immune failure. Rheumatoid arthritis and osteoporosis are associated with systemic bone loss and occur more frequently in old age. It is known that premature immunosenescence contributes to the pathogenesis of RA whereas its role for the evolvement of bone loss is not well understood. I worked on the hypothesis that aging of T cells is linked with bone loss. For this reason, we examine the prevalence of aged T cells in patients with RA with and without bone loss. In functional assays we test the mechanisms how aged T cells might induce bone resorption.Methods41 patients underwent measurement of bone density. The prevalence of naive, memory and CD28- among the CD4+ and CD8+ populations were determined by flow cytometry. In addition to staining resting cells for RANKL, RANKL expression was measured after cell culture with several stimulants. ResultsThe prevalence of CD4+CD28- and CD8+CD28- T cells in our RA cohort was 1.4% and 41.7%. RANKL was more frequently expressed on CD4+CD28- T cells compared to naive and memory T cells. In contrast, CD8+CD28- T cells expressed RANKL less frequently than naïve and memory CD8+ T cells. Furthermore, a significant increase of the number of RANKL+ T cells was noted after stimulation with IL-15. This increase was mainly observed in memory and CD28- T cells.The levels of circulating CD4+CD28- were inversely correlated with the results of the DEXA measurement, whereas for the CD8+CD28- T cell population we observed a trend only. Patients with reduced bone mass showed a higher prevalence of CD4+CD28- T cells compared to patients with normal bone mass. ConclusionAged CD4+CD28- T cells are associated with the occurrence of bone loss in RA. As CD4+CD28- T cells express surface RANKL more frequently than other CD4+ subsets, a direct influence of these cell population in the pathogenesis of osteoclastogenesis is possible.