Evidence map›Paper›PMID 25568177›Full record

ArticleJournal of the American Society of Nephrology : JASN2015

Role of Myeloid-Derived Suppressor Cells in Glucocorticoid-Mediated Amelioration of FSGS.

Limin Li, Tao Zhang, Wenli Diao, Fangfang Jin, Lei Shi, Jiao Meng, Huan Liu, Jing Zhang, Cai-Hong Zeng, Ming-Chao Zhang and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

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  13. Monocytic Myeloid Derived Suppressor Cells in Hematological Malignancies.International journal of molecular sciences · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Immunology of idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2018
    Review
  18. Article
  19. Review
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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

15 authors at 6 institutions in 3 countries.

Limin LiState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China;
Tao ZhangNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and.
Wenli DiaoState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China;
Fangfang JinState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China;
Lei ShiState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China; Center for Inflammation, Immunity and Infection, Department of Biology, Georgia State University, Atlanta, Georgia.
Jiao MengNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and.
Huan LiuState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China;
Jing ZhangState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China;
Cai-Hong ZengNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and.
Ming-Chao ZhangNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and.
Shaoshan LiangNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and.
Yuan LiuCenter for Inflammation, Immunity and Infection, Department of Biology, Georgia State University, Atlanta, Georgia.
Chen-Yu ZhangState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China; liuzhihong@nju.edu.cn kzen@nju.edu.cn cyzhang@nju.edu.cn.
Zhihong LiuNational Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and liuzhihong@nju.edu.cn kzen@nju.edu.cn cyzhang@nju.edu.cn.
Ke ZenState Key Laboratory of Pharmaceutical Biotechnology, Jiangsu Engineering Research Center for MicroRNA Biology, Nanjing, China; National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University School of Medicine, Nanjing, China; and liuzhihong@nju.edu.cn kzen@nju.edu.cn cyzhang@nju.edu.cn.
Nanjing General Hospital of Nanjing Military Command · CNPharmaceutical Biotechnology (Czechia) · CZState Key Laboratory of Pharmaceutical BiotechnologyChina Pharmaceutical University · CNNanjing University · CNGeorgia State University · US

Funding

Regulating neutrophil response during chronic inflammation through SIRPa alteratiR01AI106839 · NIAID · GEORGIA STATE UNIVERSITY · PI LIU, YUAN · 2014 to 2018
$2.0M
NIAID NIH HHS R01 AI106839
6 · The paper itself

Abstract

The mechanism by which glucocorticoids alleviate renal inflammatory disorders remains incompletely understood. Here, we report that the efficacy of glucocorticoids in ameliorating FSGS depends on the capacity to expand myeloid-derived suppressor cells (MDSCs). After glucocorticoid treatment, the frequency of CD11b(+)HLA-DR(-)CD14(-)CD15(+) MDSCs in peripheral blood rapidly increased in patients with glucocorticoid-sensitive FSGS but remained unchanged in patients with glucocorticoid-resistant FSGS. The frequency of CD11b(+)Gr-1(+) MDSCs in mouse peripheral blood, bone marrow, spleen, kidney-draining lymph nodes (KDLNs), and kidney also increased after glucocorticoid treatment. The induced MDSCs from glucocorticoid-treated mice strongly suppressed T cells, dendritic cells, and macrophages but induced regulatory T cells in spleen, KDLNs, and kidney. Moreover, glucocorticoid treatment suppressed doxorubicin-induced T cell proliferation, dendritic cell and macrophage infiltration, and proinflammatory cytokine production, whereas this protective effect was largely abolished by depleting MDSCs using anti-Gr-1 antibody. Finally, the adoptive transfer of induced MDSCs into the doxorubicin-treated mice not only confirmed the protective role of MDSCs in doxorubicin-induced renal injury but also showed that the transferred MDSCs rapidly migrated into the lymphocyte-accumulating organs, such as the spleen and KDLNs, where they suppressed T cell proliferation. Taken together, these results demonstrate that glucocorticoid treatment ameliorates FSGS by expanding functional MDSCs and that this rapid elevation of MDSCs in peripheral blood may serve as an indicator for predicting the efficacy of glucocorticoid treatment.

Indexed as

AdolescentAdoptive TransferAdultAnimalsAntigens, LyCD11b AntigenCell CountCell MovementCell ProliferationDendritic CellsDoxorubicinFemaleGlomerulosclerosis, Focal SegmentalGlucocorticoidsHLA-DR AntigensHumansAntigens, LyCD11b AntigenDoxorubicinGlucocorticoidsGr-1 protein, mouseHLA-DR AntigensLewis X AntigenLipopolysaccharide ReceptorsLy-6C antigen, mouseReceptors, Chemokinecell activationchemokinefocal segmental glomerulosclerosislymphocytesrenal protection

Identifiers

PMID25568177
PMCPMC4552109
OpenAlexW2160350015

What OpenQuestion holds

Textmetadata
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.