Evidence map›Paper›PMID 35895513›Full record

ArticleBlood advances2023

Granulocytic myeloid-derived suppressor cells to prevent and treat murine immune-mediated bone marrow failure.

Xingmin Feng, Jisoo Kim, Gladys Gonzalez-Matias, Nidhi Aggarwal, Ash Lee Manley, Zhijie Wu, Sabrina Solorzano, Sai Batchu, Shouguo Gao, Jichun Chen and 1 more

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 12 citations in OpenAlex.

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  8. Influence of Housing Temperature and Genetic Diversity on Allogeneic T Cell-Induced Tissue Damage in Mice.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Xingmin FengHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0001-8018-2366
Jisoo KimHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Gladys Gonzalez-MatiasHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Nidhi AggarwalHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0002-2906-9920
Ash Lee ManleyHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Zhijie WuHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0003-3984-0819
Sabrina SolorzanoHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Sai BatchuHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.ORCID 0000-0003-1531-9682
Shouguo GaoHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Jichun ChenHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
Neal S YoungHematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD.
National Institutes of Health · US

Funding

Pathogenesis And Treatment Of Aplastic AnemiaZIAHL002315 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI YOUNG, NEAL S · 2009 to 2025
$60.1M
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells that originate in the bone marrow (BM) and have immunoregulatory functions. MDSCs have been implicated in the pathogenesis of several autoimmune diseases but have not been investigated in immune aplastic anemia (AA). We examined the roles of granulocytic-MDSCs (G-MDSCs) in murine models of human AA and BM failure (BMF). As both prophylaxis and therapy, BM-derived G-MDSCs improved pancytopenia and BM cellularity and suppressed BM T-cell infiltration in major histocompatibility complex (MHC)-matched C.B10 BMF mice. These effects were not obtained in the MHC-mismatched CByB6F1 AA model, likely because of MHC disparity between G-MDSCs and donor T cells. Single-cell RNA sequencing demonstrated that G-MDSCs downregulated cell cycle-related genes in BM-infiltrated T cells, consistent with suppression of T-cell proliferation by G-MDSCs through reactive oxygen species pathways. Clearance of G-MDSCs in the MHC-mismatched CByB6F1 model using anti-Ly6G antibody facilitated T cell-mediated BM destruction, suggesting an intrinsic immunosuppressive property of G-MDSCs. However, the same anti-Ly6G antibody in the MHC-matched C.B10 AA model mildly mitigated BMF, associated with expansion of an intermediate Ly6G population. Our results demonstrate that G-MDSC eradication and therapeutic efficacy are immune context-dependent.

Indexed as

Anemia, AplasticMyeloid-Derived Suppressor CellsPancytopeniaAnimalsBone Marrow Failure DisordersGranulocytesHumansMiceMyeloid Cells

Identifiers

PMID35895513
PMCPMC9827041
OpenAlexW4288051574

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.