Evidence map›Paper›PMID 34326171›Full record

ArticleJournal for immunotherapy of cancer2021

Overexpression of CD200 is a Stem Cell-Specific Mechanism of Immune Evasion in AML.

Shelley Herbrich, Natalia Baran, Tianyu Cai, Connie Weng, Marisa J L Aitken, Sean M Post, Jared Henderson, Chunhua Shi, Guillame Richard-Carpentier, Guy Sauvageau and 6 more

Erratum issuedOpen access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal for immunotherapy of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 40 citations in OpenAlex.

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  2. Refining favorable-risk classification in pediatricBlood science (Baltimore, Md.) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 3 countries.

Shelley HerbrichDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.ORCID 0000-0002-3825-6752
Natalia BaranDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Tianyu CaiDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Connie WengDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Marisa J L AitkenDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Sean M PostDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Jared HendersonDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Chunhua ShiOncology Research for Biologics and Immunotherapy Translation (ORBIT) platform, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Guillame Richard-CarpentierDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Guy SauvageauUniversity of Montreal Institute for Research in Immunology and Cancer, Montreal, Quebec, Canada.
Keith BaggerlyDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Gheath Al-AtrashDepartment of Stem Cell Transplantation and Cellular Therapy, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
R Eric DavisDepartment of Lymphoma and Myeloma, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Naval DaverDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Dongxing ZhaOncology Research for Biologics and Immunotherapy Translation (ORBIT) platform, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Marina KonoplevaDepartment of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA mkonople@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USCharles University · CZInstitute for Research in Immunology and Cancer · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) stem cells (LSCs) are capable of surviving current standard chemotherapy and are the likely source of deadly, relapsed disease. While stem cell transplant serves as proof-of-principle that AML LSCs can be eliminated by the immune system, the translation of existing immunotherapies to AML has been met with limited success. Consequently, understanding and exploiting the unique immune-evasive mechanisms of AML LSCs is critical.

methodsAnalysis of stem cell datasets and primary patient samples revealed CD200 as a putative stem cell-specific immune checkpoint overexpressed in AML LSCs. Isogenic cell line models of CD200 expression were employed to characterize the interaction of CD200

resultsOur results demonstrate that CD200 is selectively overexpressed in AML LSCs and is broadly immunosuppressive by impairing cytokine secretion in both innate and adaptive immune cell subsets. In a PBMC-humanized mouse model, CD200

conclusionsOverexpression of CD200 is a stem cell-specific marker that contributes to immunosuppression in AML by impairing effector cell metabolism and function. CD200 antibody therapy is capable of simultaneously reducing CD200-mediated suppression while also engaging macrophage activity. This study lays the groundwork for CD200-targeted therapeutic strategies to eliminate LSCs and prevent AML relapse.

Indexed as

AnimalsAntigens, CDHumansImmune EvasionLeukemia, Myeloid, AcuteMiceMice, Inbred NODAntigens, CDantigens, CD200immunomodulationlymphocyte activationmetabolic networks and pathwaystumor escape

Identifiers

PMID34326171
PMCPMC8323398
OpenAlexW3186632176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.