A panoramic landscape of the human hematopoietic system is established and its lifelong behaviors are elaborated, in which a steady-state reference enabled the delineation of pathological hallmarks across hematological malignancies.
Abstract
Single-cell technologies have transformed our view of normal and malignant hematopoiesis, yet a framework linking lifelong homeostatic hematopoiesis to hematological diseases in blood ecosystem remains incomplete. Here, we constructed a high-resolution landscape of the entire hematopoietic system by integrating transcriptomes of ∼1 million cells from 207 healthy samples spanning five developmental stages (fetal, neonatal, childhood, adult, elderly), and identified 96 blood cell clusters, including a VNN2-marked monocyte subset in the fetus and TSHZ2-marked T cell subsets exhibiting distinct age-dependent dynamics. We uncovered a reversal in hematopoietic stem cell/multipotent progenitor (HSC/MPP) stemness around childhood and a postnatal lymphoid bias shift from reduced early B/T lineage potential to enhanced natural killer (NK) cytotoxicity, coordinately orchestrated by intracellular transcription factor activity and intercellular interactions. Projecting 116 pan-malignancy samples (9 hematological malignancies) to our refined blood cell reference, we identified the upregulation of MYC and MHC II signaling as relatively conserved features correlating with poor prognosis, while hematopoiesis-related modules exhibited subtype-specific distributions with divergent clinical implications. Importantly, we developed a prognostic framework incorporating two core signatures shared across hematological malignancies and subtype-specific features. We further revealed an antagonism between inflammatory and cytotoxic programs across malignancies. Together, we established a panoramic landscape of the human hematopoietic system and elaborated its lifelong behaviors, in which a steady-state reference enabled the delineation of pathological hallmarks across hematological malignancies.
This study provides a high-resolution transcriptional atlas of canine hematopoiesis and highlights conserved regulatory programs between dogs and humans, offering a reference for future studies of hematologic disease and cross-species comparisons.
Dylan T. Ammons, Christopher Contursi, McKenzie Olsen et al.· Scientific Reports· 2 citations
A Cellular Indexing of Transcriptomes and Epitopes by sequencing (CITE-seq) based atlas of 9,281 low-frequency mouse BM HSPCs, profiled using a 123 antibody-derived tag panel coupled with genome-wide single-cell transcriptomes, enables exploration of mouse hematopoietic progenitor states driving discoveries in hematolo...
M. Bhuyan, S. Barman, Shafaqat Ali et al.· bioRxiv· 0 citations
Neonatal sepsis remains a leading cause of infant mortality, yet mechanisms driving concurrent hyperinflammation and immunosuppression remain unclear. Here, we perform single-cell RNA sequencing on 26 blood samples from 18 neonates, spanning acute sepsis, convalescence, and healthy controls. We identify 57 cell subtype...
Jie Wang, Ying Chen, Pei-Cen Zou et al.· Cell Reports· 0 citations
Hematopoietic stem cells (HSCs) sustain lifelong hematopoiesis as their progeny differentiate into all blood cell lineages. Homeostatic HSCs are mostly quiescent and only rarely divide, however their proliferation and differentiation rates can be modulated by external factors. Acute and chronic infections from a wide r...
Christiana Georgiou, Qi Liu, Federica Bruno et al.· Blood· 0 citations
In insight into HSC aging, Pbx1 is identified as a key regulator of these age-related transcriptional and differentiation changes and may inform approaches to modulate age-associated HSC dysfunction.
A niche-mimetic culture system that integrates intrinsic and extrinsic bone marrow regulatory cues, including pharmacologic inhibition of the m6A reader YTHDF2 using the small molecule Y13-27, a three-dimensional microenvironment, and N-cadherin-mediated adhesion is established that preserves transcriptional and epigen...
Xinjian Mao, Ning Zhang, Xi C. He et al.· Blood· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.