The current thesis aimed at broadening our understanding of the processes governing stress erythropoiesis. Phenylhydrazine-induced haemolytic anaemia was utilised as a mouse model of acute stress erythropoiesis. An unbiased whole transcriptome analysis followed by a multi-parametric flow cytometry assessment of splenic stress erythroid precursors was performed. Here, it is identified for the first time, a subpopulation of erythroid precursors in the steady state spleen, which express a broad range of immune-related cell surface markers. These unique steady state splenic cells were termed ISEPs (Immune-marker- expressing Splenic Erythroid Precursors) and are hypothesised to represent potential stress erythroid progenitors. The concept of a possible ‘erythroid synapse’ between these ISEPs and erythroblastic island (EBI) macrophages was introduced. The existence of a specialised stress EBI that holds these ISEPs in a ‘dormant’ state during steady state conditions via the ‘erythroid synapse’ was postulated. It was shown that there is both a downregulation of immune marker mRNA and a significantly reduced frequency of ISEPs during stress erythropoiesis in mice. Downregulation of immune markers during stress erythropoiesis may result in a breakdown of the postulated stress EBIs, allowing unfettered accelerated proliferation and maturation of ISEPs during stress erythropoiesis. Mouse pregnancy was also shown to induce stress erythropoiesis. ISEPs were again depleted on examining the splenic niche erythroid precursor component in pregnant mice. In the non-pregnancy setting, there were hints of a greater erythroid stress response in female mice compared to male mice, and it was questioned whether this was an oestrogen-mediated effect. It is hoped that the insights gained from this thesis will be built on to further uncover the function and regulation of ISEPs, and thereby assist with treatment of human conditions displaying stress erythropoiesis.