Interferon-γ mediates suppression of erythropoiesis but not reduced red cell survival following CpG-ODN administration in vivo

Isocitrate ameliorates anemia by suppressing the erythroid iron restriction response

“…Third, IC conferred resistance to IFN-γ and TNF-α under conditions of iron restriction (Figure 2A and Supplemental Figure 4). The relevance of these findings to ACDI is suggested by prior implication of IFN-γ in erythropoietic repression in human chronic kidney disease and in multiple animal models of anemia (22,27,28). In addition, IFN-signaling pathways are known to participate in erythroid inhibition by TNF-α and IL-1 and in human idiopathic refractory anemia (29,30).…”

Chronic IFN-γ production in mice induces anemia by reducing erythrocyte life span and inhibiting erythropoiesis through an IRF-1/PU.1 axis

“…36 However, this study addressed the role of IFN-␥ in acute inflammatory responses, whereas we have used a valid model for chronic inflammation. We hypothesized that a chronic response could result in macrophage activation and thereby affect RBC uptake.…”

CpG-ODN 2006 and human parvovirus B19 genome consensus sequences selectively inhibit growth and development of erythroid progenitor cells

“…Sparwasser et al 15 demonstrated that unmethylated CpG-ODN 2006 triggered extramedullary hematopoiesis by promoting expansion of granulocytemacrophage colony forming units (CFUs) and early erythroid progenitors, and that enhanced splenic hematopoiesis is the result of CpG-ODN-induced cytokines that mobilize bone marrow progenitor cells to the spleen. Subsequently, Thawani et al 16 showed that in vivo administration of unmethylated CpG-ODN exerted anemia in mice. They reported that this CpG-ODNinduced suppression was indirect and required accessory cells, including antigen-presenting cells (APCs), which activated other cells to produce proinflammatory cytokines, and IFN-␥ was the major factor mediating erythropoietic suppression.…”