This thesis investigated the effect of acute psychological stress and (beta)-adrenergic receptor ((beta)AR) stimulation on the mobilization of CD8+ T lymphocytes (CD8TLs) and progenitor cell (PC) populations. Chapter 2 demonstrated that CD8TL stress- and (beta)AR- sensitivity increases in parallel with greater effector functions and cell differentiation. As Cytomegalovirus (CMV) infection influences CD8TL differentiation, Chapter 3 compared the mobilization of cytotoxic lymphocytes in CMV seropositive and seronegative individuals; CMV infection enhanced the stress reactivity of CD8TLs, CD4TLs and NKT-like cells. Chapter 4 examined whether antigen-specificity could modulate CD8TL stress- and (beta)AR-sensitivity. CMV-specific cells demonstrated enhanced mobilization compared to the total-memory CD8TL and the total Epstein-Barr virus (EBV) population. In Chapter 5, we demonstrated that PC subsets, capable of both replenishing leukocyte populations and maintaining endothelial integrity, were also mobilized by acute psychological stress. This result was not replicated by (beta)ARagonist infusion suggesting the involvement of (alpha)AR or non-adrenergic mechanism. In sum, the current findings suggest that stress mobilization serves to protect the host by increasing immune protection and tissue repair mechanisms. However, such a response may also be detrimental dependent on the circumstance, i.e., infection versus inflammation.