Interferon‐γ Mediates Anemia but Is Dispensable for Fulminant Toll‐like Receptor 9–Induced Macrophage Activation Syndrome and Hemophagocytosis in Mice

Abstract

These data demonstrate that both fulminant MAS and hemophagocytosis can arise independently of IFNγ, IL-12, or type I IFNs. They also suggest that IFNγ-mediated dyserythropoiesis, not hemophagocytosis, is the dominant cause of anemia in fulminant TLR-9-induced MAS. Thus, our data establish a novel mechanism for the acute anemia of inflammation, but suggest that a variety of triggers can result in hemophagocytic disease.