Functionally Distinct Subsets of Lineage-Biased Multipotent Progenitors Control Blood Production in Normal and Regenerative Conditions
Open accessAbstract
Despite great advances in understanding the mechanisms underlying blood production, lineage specification at the level of multipotent progenitors (MPPs) remains poorly understood. Here, we show that MPP2 and MPP3 are distinct myeloid-biased MPP subsets that work together with lymphoid-primed MPP4 cells to control blood production. We find that all MPPs are produced in parallel by hematopoietic stem cells (HSCs), but with different kinetics and at variable levels depending on hematopoietic demands. We also show that the normally rare myeloid-biased MPPs are transiently overproduced by HSCs in regenerating conditions, hence supporting myeloid amplification to rebuild the hematopoietic system. This shift is accompanied by a reduction in self-renewal activity in regenerating HSCs and reprogramming of MPP4 fate toward the myeloid lineage. Our results support a dynamic model of blood development in which HSCs convey lineage specification through independent production of distinct lineage-biased MPP subsets that, in turn, support lineage expansion and differentiation.
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MPPGM appears to be a nexus of myeloid expansion under both inflammatory conditions and in animal models of myeloid malignancy.
“It is noteworthy that MPPGM (also commonly referred to as MPP3) (Challen et al., 2021) appears to be a nexus of myeloid expansion under both inflammatory conditions and in animal models of myeloid malignancy (Schepers et al., 2013; Pietras et al., 2015; Shih et al., 2015; Pietras et al., 2016; Herault et al., 2017; Hernandez et al., 2020; Kang et al., 2020; Rabe et al., 2020).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Pietras et al., 2015
The Results (Contribution to blood regeneration; page unavailable) identify MPP2 and MPP3 as a rapidly emerging compartment of myeloid amplification after transplantation, supporting a role for MPP3 in myeloid expansion. The paper does not establish that MPP3 has this role under inflammatory conditions or in animal models of myeloid malignancy; its discussion of increased IL-6 concerns MPP4. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPU.1 deficiency leads to overproduction of mature myeloid cells and aberrant expansion of MPPGM following chronic IL-1β treatment.
“We find that PU.1 deficiency leads to overproduction of mature myeloid cells and aberrant expansion of MPPGM, a progenitor population that serves as an “emergency” reservoir for myeloid cell production (Pietras et al., 2015), following chronic IL-1β treatment.”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Pietras et al., 2015
Coupling gene expression variation with assessment of different subpopulations has enabled distinct functional groups to be defined.
“Coupling gene expression variation with assessment of different subpopulations has enabled distinct functional groups to be defined (Pietras et al., 2015).”
From Unraveling Hematopoiesis through the Lens of Genomics (2020) · cites this paper as Pietras et al., 2015
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“under both inflammatory conditions and in animal models of myeloid malignancy (Schepers et al., 2013; Pietras et al., 2015; Shih et al., 2015; Pietras et al., 2016; Herault et al., 2017; Hernandez et al., 2020; Kang et al., 2020; Rabe et al., 2020).”
BackgroundMethodResultInfluentialSelf-citationG2 arrest primes hematopoietic stem cells for megakaryopoiesis
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- Authors
- Pietras, E. M., Reynaud, D., Kang, Y.-A., Carlin, D., Calero-Nieto, F. J., Leavitt, A. D., Stuart, J. M., Göttgens, B., & Passegué, E.
- Affiliations
- University of California, San Francisco (US)
- University of California, Santa Cruz (US)
- Wellcome/MRC Cambridge Stem Cell Institute (GB)
- ORCID
- Venue
- Cell stem cell
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 17
- Issue
- 1
- Pages
- 35-46
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- PMC
- PMC4542150
- OpenAlex
- W2104994033
- Cited by
- 723
- References
- 41
- Citations by year
- 2026: 50 · 2025: 86 · 2024: 81 · 2023: 86 · 2022: 94 · 2021: 81 · 2020: 86 · 2019: 54 · 2018: 46 · 2017: 35 · 2016: 20 · 2015: 2 · 2014: 1
- FWCI
- 26.95
- Type
- journal article
- Language
- en
- Update notices
- erratum (2015-08-06)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Apollo (University of Cambridge) (acceptedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Leukemia and Lymphoma Society
- Wellcome Trust (97922)
- Cancer Research UK (12765)
- Leukaemia and Lymphoma Research
- National Institutes of Health
- University of California, San Francisco
- Medical Research Council (MR/M008975/1, MC_PC_12009)
- Biotechnology and Biological Sciences Research Council (BB/I00050X/1)
- National Heart, Lung, and Blood Institute (R01HL092471, F32HL106989)
- National Cancer Institute (R01CA180778)
- National Institute of General Medical Sciences (R01GM109031)
- National Institute of Allergy and Infectious Diseases (T32AI007334)
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK098315)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Keywords
- multipotent progenitors, hematopoietic stem cells, lineage specification, hematopoietic regeneration, self-renewal, blood development, hematopoiesis
- MeSH terms
- Animals, Cell Differentiation, Hematopoiesis, Hematopoietic Stem Cells, Mice, Inbred C57BL, Mice, Transgenic, Models, Biological, Regeneration, Gene Expression, Cell Lineage, Myeloid Progenitor Cells, Multipotent Stem Cells, Mice, Lymphoid Progenitor Cells, Cellular Reprogramming
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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