Acute anaemia induces erythroid progenitors to migrate from the bone marrow to the spleen, a secondary site of erythrocyte production, in a process termed stress erythropoiesis. The massive changes in whole body physiology that accompanies pregnancy lead to acute anaemia. We therefore asked whether pregnancy induces stress erythropoiesis in the mouse. Acute haemolytic anaemia, induced by injection of phenylhydrazine (PHZ) was used as a comparative model of stress erythropoiesis. The surface phenotype of erythroblasts in virgin, pregnant, PBS and PHZ-treated animals was assessed by flow cytometry. Splenomegaly was observed in pregnant animals, peaking when the embryos were at E9.5-13.5. The degree of splenomegaly in pregnancy was less severe than that seen in PHZ-treated animals. However, we did observe reticulocytosis and an increased frequency in erythroblasts expressing a4-, a5-, and b1-integrin in splenic erythroblasts from pregnant animals, indicative of stress erythroblast migration from the bone marrow. In both PHZ-induced and pregnancy-induced stress erythropoiesis we observed that stress erythroblasts lacked high surface CD45 expression that was observed on normal erythroblasts. CD45, a tyrosine phosphatase, is a known inhibitor of Janus kinase 2 (JAK2), which is involved in the JAK2-signal transducer and activator of transcription 5 (JAK2-STAT5) signalling pathway. This pathway plays an essential role in erythropoiesis promoted by erythropoietin. We propose that pregnancy may represent a physiological scenario where stress erythropoiesis occurs and that CD45 is down regulated both in pregnancy as well as in PHZ induced stress erythropoiesis, to enhance erythroblast production. Acute anaemia induces erythroid progenitors to migrate from the bone marrow to the spleen, a secondary site of erythrocyte production, in a process termed stress erythropoiesis. The massive changes in whole body physiology that accompanies pregnancy lead to acute anaemia. We therefore asked whether pregnancy induces stress erythropoiesis in the mouse. Acute haemolytic anaemia, induced by injection of phenylhydrazine (PHZ) was used as a comparative model of stress erythropoiesis. The surface phenotype of erythroblasts in virgin, pregnant, PBS and PHZ-treated animals was assessed by flow cytometry. Splenomegaly was observed in pregnant animals, peaking when the embryos were at E9.5-13.5. The degree of splenomegaly in pregnancy was less severe than that seen in PHZ-treated animals. However, we did observe reticulocytosis and an increased frequency in erythroblasts expressing a4-, a5-, and b1-integrin in splenic erythroblasts from pregnant animals, indicative of stress erythroblast migration from the bone marrow. In both PHZ-induced and pregnancy-induced stress erythropoiesis we observed that stress erythroblasts lacked high surface CD45 expression that was observed on normal erythroblasts. CD45, a tyrosine phosphatase, is a known inhibitor of Janus kinase 2 (JAK2), which is involved in the JAK2-signal transducer and activator of transcription 5 (JAK2-STAT5) signalling pathway. This pathway plays an essential role in erythropoiesis promoted by erythropoietin. We propose that pregnancy may represent a physiological scenario where stress erythropoiesis occurs and that CD45 is down regulated both in pregnancy as well as in PHZ induced stress erythropoiesis, to enhance erythroblast production.