Figure 3. Aged thymus is dysfunctional. With advancing age, thymus loses its cellularity while accumulating adipocytes and fibroblasts. Aged thymus develops an inflammatory environment with high levels of oxidative stress. This is evident by the accumulation of senescent TECs with elevated markers of DNA damage and oxidative stress. Despite the adequate recruitment of T-cell progenitors, aged thymus generates inadequate number of naïve T-cells which leads to the age-associated depletion of TCR repertoire and ultimately a change in the immune cell landscape. Due to the impaired negative selection of dysfunctional T-cells, the aged thymus shows an increase in the output of dysfunctional and autoreactive T-cells leading to the establishment of low-grade chronic inflammation. Abbreviations: SnC: Senescent cell; SASP: Senescence associated secretory phenotype; ROS: Reactive Oxygen Species; TEC: Thymic epithelial cell; TCR: T-cell receptor.