The thymus, which is the primary site for T cell maturation, begins to involute after puberty leading to defects in T cell function. Although the mechanisms of thymic atrophy/involution are not clearly understood, both LPCs and stem cell niche aging have been proposed to be the cause. There are numerous studies in lympho-hematopoietic progenitor cells (LPC), along with a few studies dealing with stem cell niche ageing; however, there is a scarcity of studies that combine the interaction of the two. The lack of models seems to be a contributing factor to the scarcity of a combined study. Age-related T-cell immune system defects are associated with developmental disabilities in the interaction of progenitors in the bone marrow (BM) and thymic niches. So far what is known is that both cellular components will ultimately develop intrinsic/irreversible defects. There is much debate about which component is primarily responsible for the initial events that lead to the adverse regulation of the other component, but understanding the relationship is of clinical relevance for rejuvenating the aged immune system in order to delay/treat the onset of age-related diseases. In order to address the role of LPCs and stem cell niche aging, we have developed several comprehensive in vivo and in vitro models for functional characterizations of the lymphostromal interaction in mice. By using BM transplantation from wild type donors along with an IL7R ^-/- mouse as a recipient/host, transplantation of a fetal thymus into one/two hosts to recruit naturally thymic-seeding LPCs from young and/or aged BM in vivo, we found that LPCs outlive their niche cells in the BM and thymus. Although aged LPCs cannot compete against their younger counterparts, this is reversible when a young microenvironment is provided. Therefore, aging of T-lineage stem cells is largely regulated by their niches.