02005nas a2200349   4500000000100000000000100001008004100002260001500043653001900058653002000077100001100097700001400108700001300122700001500135700001300150700001700163700001100180700001500191700002500206700001800231700002300249700001400272700002200286700002100308700001400329700001200343245009100355856005500446300000900501520113100510022001401641       2026                            d  c2026-07-0210aRNA sequencing10aTranscriptomics1 aXu Han1 aKehan Ren1 aPan Wang1 aHonghao Bi1 aErmin Li1 aInci Aydemir1 aAmy Ji1 aWenjie Cai1 aLaya Soleimanisardoo1 aChing Man Wai1 aMatthew J. Schipma1 aYijie Liu1 aJeffery Goldstein1 aMadina Sukhanova1 aJing Yang1 aPeng Ji00aSpatial transcriptomic analyses highlight distinct erythroid niches in mice and humans  uhttps://www.nature.com/articles/s41588-026-02671-2  a1-123 aErythroid cells require specialized microenvironments called erythroblastic islands (EBIs), niches comprising a central macrophage surrounded by developing erythroid precursors, to complete their maturation. Understanding EBI composition and function has been limited by two-dimensional in vitro models and the unclear composition of EBIs in human hematopoietic tissues. Using spatial transcriptomic mapping in mouse and human hematopoietic tissues during development and under stress conditions, we show that EBI architecture is unexpectedly species-specific. In mice, C1q-expressing macrophages serve as a hallmark of EBI central macrophages and mediate clearance of ejected erythroid nuclei. In humans, however, EBIs are characterized by macrophage-independent erythroid clusters in fetal liver and bone marrow, whose integrity depends critically on the adhesion molecule ICAM4. These human erythroid clusters are disrupted in myeloid diseases but can be restored with therapy. These findings redefine conventional models of erythroid niche biology and establish a framework for understanding niche dynamics across species.  a1546-1718