Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLE
Erythroid mitochondrial retention triggers myeloid-dependent type I interferon in human SLEA subgroup of SLE patients fail to engage HIF-regulated metabolic and proteasomal pathways causing the accumulation of mitochondria-containing red blood cells. These cells, when engulfed by macrophages, activate cGAS/STING-dependent inflammation.A subgroup of SLE patients fail to engage HIF-regulated metabolic and proteasomal pathways causing the accumulation of mitochondria-containing red blood cells. These cells, when engulfed by macrophages, activate cGAS/STING-dependent inflammation.Simone Caielli, Jacob Cardenas, Adriana Almeida de Jesus, Jeanine Baisch, Lynnette Walters, Jean Philippe Blanck, Preetha Balasubramanian, Cristy Stagnar, Marina Ohouo, Seunghee Hong, Lorien Nassi, Katie Stewart, Julie Fuller, Jinghua Gu, Jacques F. Banchereau, Tracey Wright, Raphaela Goldbach-Mansky, Virginia Pascualhttps://secure.jbs.elsevierhealth.com/action/getSharedSiteSession?redirect=https%3A%2F%2Fwww.cell.com%2Fcell%2Ffulltext%2FS0092-8674%2821%2900880-1%3Frss%3Dyes&rc=0http://www.cell.com/cell/inpress.rssCellCell RSS feed.Wireless News CampaignAugust 12, 2021
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