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.

Objectives
Stimuli that activate the sympathetic nervous system, such as acute psychological stress, rapidly invoke a robust mobilization of lymphocytes into the circulation. Experimental animal studies suggest that bone marrow-derived progenitor cells (PCs) also mobilize in response to sympathetic stimulation. Here we tested the effects of acute psychological stress and brief pharmacological β-adrenergic (βAR) stimulation on peripheral PC numbers in humans.
Methods
In two studies, we investigated PC mobilization in response to an acute speech task (n=26) and βAR-agonist (isoproterenol) infusion (n=20). A subset of 8 participants also underwent the infusion protocol with concomitant administration of the βAR-antagonist propranolol. Flow cytometry was used to enumerate lymphocyte subsets, total progenitor cells, total haematopoietic stem cells (HSC), early HSC (multi-lineage potential), late HSC (lineage committed), and endothelial PCs (EPCs).
Results
Both psychological stress and βAR-agonist infusion caused the expected mobilization of total monocytes and lymphocytes and CD8+ T lymphocytes. Psychological stress also induced a modest, but significant, increase in total PCs, HSCs, and EPC numbers in peripheral blood. However, infusion of a βAR-agonist did not result in a significant change in circulating PCs.
Conclusion
PCs are rapidly mobilized by psychological stress via mechanisms independent of βAR-stimulation, although the findings do not exclude βAR-stimulation as a possible cofactor. Considering the clinical and physiological relevance, further research into the mechanisms involved in stress-induced PC mobilization seems warranted.