Evidence map›Paper›PMID 34917079›Full record

ArticleFrontiers in immunology2021

Early Myeloid Derived Suppressor Cells (eMDSCs) Are Associated With High Donor Myeloid Chimerism Following Haploidentical HSCT for Sickle Cell Disease.

Deepali K Bhat, Purevdorj B Olkhanud, Arunakumar Gangaplara, Fayaz Seifuddin, Mehdi Pirooznia, Angélique Biancotto, Giovanna Fantoni, Corinne Pittman, Berline Francis, Pradeep K Dagur and 4 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Deepali K BhatCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Purevdorj B OlkhanudCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Arunakumar GangaplaraCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Fayaz SeifuddinBioinformatics and Computational Biology Core Facility, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Mehdi PiroozniaBioinformatics and Computational Biology Core Facility, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Angélique BiancottoCenter for Human Immunology, Autoimmunity, and Inflammation, National Institutes of Health (NIH), Bethesda, MD, United States.
Giovanna FantoniCenter for Human Immunology, Autoimmunity, and Inflammation, National Institutes of Health (NIH), Bethesda, MD, United States.
Corinne PittmanCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Berline FrancisCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
Pradeep K DagurFlow Cytometry Core, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda MD, United States.
Ankit SaxenaFlow Cytometry Core, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda MD, United States.
J Philip McCoyFlow Cytometry Core, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda MD, United States.
Ruth M PfeifferDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD, United States.
Courtney D FitzhughCellular and Molecular Therapeutics Branch, National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, MD, United States.
National Institutes of Health · USNational Heart Lung and Blood Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Haploidentical hematopoietic stem cell transplantation (haplo-HSCT) is a widely available curative option for patients with sickle cell disease (SCD). Our original non-myeloablative haplo-HSCT trial employing post-transplant (PT) cyclophosphamide had a low incidence of GVHD but had high rejection rates. Here, we aimed to evaluate immune reconstitution following haplo-HSCT and identify cytokines and cells associated with graft rejection/engraftment. 50 cytokines and 10 immune cell subsets were screened using multiplex-ELISA and flow cytometry, respectively, at baseline and PT-Days 30, 60, 100, and 180. We observed the most significant differences in cytokine levels between the engrafted and rejected groups at PT-Day 60, corresponding with clinical findings of secondary graft rejection. Of the 44 cytokines evaluated, plasma concentrations of 19 cytokines were different between the two groups at PT-Day 60. Factor analysis suggested two independent factors. The first factor (IL-17A, IL-10, IL-7, G-CSF, IL-2, MIP-1a, VEGF, and TGFb1 contributed significantly) was strongly associated with engraftment with OR = 2.7 (95%CI of 1.4 to 5.4), whereas the second factor (GROa and IL-18 contributed significantly) was not significantly associated with engraftment. Sufficient donor myeloid chimerism (DMC) is critical for the success of HSCT; here, we evaluated immune cells among high (H) DMC (DMC≥20%) and low (L) DMC (DMC<20%) groups along with engrafted and rejected groups. We found that early myeloid-derived suppressor cell (eMDSC) frequencies were elevated in engrafted patients and patients with HDMC at PT-Day 30 (P< 0.04 & P< 0.003, respectively). 9 of 20 patients were evaluated for the source of eMDSCs. The HDMC group had high mixed chimeric eMDSCs as compared to the LDMC group (P< 0.00001). We found a positive correlation between the frequencies of eMDSCs and Tregs at PT-Day 100 (r=0.72, P <0.0007); eMDSCs at BSL and Tregs at PT-Day 100 (r=0.63, P <0.004). Of 10 immune regulatory cells and 50 cytokines, we observed mixed chimeric eMDSCs and IL-17A, IL-10, IL-7, G-CSF, IL-2, MIP-1a, VEGF, TGFb1 as potential hits which could serve as prognostic markers in predicting allograft outcome towards engraftment following haploidentical HSCT employing post-transplant cyclophosphamide. The current findings need to be replicated and further explored in a larger cohort.

Indexed as

Hematopoietic Stem Cell TransplantationTransplantation ChimeraAdultAnemia, Sickle CellChimerismCyclophosphamideCytokinesGraft RejectionGraft SurvivalHumansImmune ReconstitutionImmunosuppressive AgentsMyeloid-Derived Suppressor CellsPrognosisTransplantation ConditioningTransplantation, HaploidenticalCyclophosphamideCytokinesImmunosuppressive Agentsdonor myeloid chimerismearly myeloid derived suppressor cellshaploidentical HSCTIL-10sickle cell diseaseTregs

Identifiers

PMID34917079
PMCPMC8669726
OpenAlexW3216863104

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Registered trials

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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.