Inflammation induces stress erythropoiesis through heme-dependent activation of SPI-C

作者：Laura F. Bennett, Chang Liao, Michael D. Quickel, Beng San Yeoh, Matam Vijay–Kumar, Pamela Hankey‐Giblin, K. Sandeep Prabhu, Robert F. Paulson · 发表于：Science Signaling · 年份：2019 · DOI：10.1126/scisignal.aap7336 · 被引用次数：91 · 研究领域：Erythrocyte Function and Pathophysiology、Heme Oxygenase-1 and Carbon Monoxide、Erythropoietin and Anemia Treatment

, both of which encode ligands that initiate the expansion of stress erythroid progenitors (SEPs) in the spleen. Furthermore, despite their inhibition of steady-state erythropoiesis in the bone marrow, the proinflammatory cytokines TNF-α and IL-1β promoted the expansion and differentiation of SEPs in the spleen. These data suggest that inflammatory signals induce stress erythropoiesis to maintain erythroid homeostasis when inflammation inhibits steady-state erythropoiesis.