Evidence map›Paper›PMID 29445144›Full record

ArticleCell death & disease2018

Lenalidomide regulates CNS autoimmunity by promoting M2 macrophages polarization.

Qinjie Weng, Jiaying Wang, Jiajia Wang, Jing Wang, Fahmida Sattar, Zhikang Zhang, Jiahuan Zheng, Zijie Xu, Mengting Zhao, Xuan Liu and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. 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 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  15. Article
  16. Review
  17. Article
  18. Article
  19. MicroRNA Regulated Macrophage Activation in Obesity.Journal of translational internal medicine · 2019
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 3 countries.

Qinjie WengInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Jiaying WangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Jiajia WangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Jing WangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Fahmida SattarInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Zhikang ZhangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Jiahuan ZhengInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Zijie XuInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Mengting ZhaoInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Xuan LiuInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Lijun YangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Guifeng HaoDepartment of Rheumatology, Zhejiang Provincial People's Hospital, Hangzhou, China.
Liang FangCancer Research Program, Max Delbrueck Center for Molecular Medicine in the Helmholtz Society, Berlin, Germany.
Q Richard LuDepartment of Pediatrics, Brain Tumor Center, Cancer and Blood Disease Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Bo YangInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. yang924@zju.edu.cn.
Qiaojun HeInstitute of Pharmacology & Toxicology, Zhejiang Province Key Laboratory of Anti-Cancer Drug Research, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China. qiaojunhe@zju.edu.cn.
Zhejiang University · CNCincinnati Children's Hospital Medical Center · USMax Delbrück Center · DEZhejiang Provincial People's Hospital · CN

Funding

Molecular Mechanisms of Oligodendrocyte Differentiation and MyelinationR01NS072427 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2010 to 2018
$3.6M
Chromatin remodeling control of myelination and remyelinationR01NS075243 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI LU, QING R · 2012 to 2018
$2.6M
Molecular and signaling mechanisms of peripheral nerve sheath tumorigenesisR37NS096359 · NINDS · CINCINNATI CHILDRENS HOSP MED CTR · PI LU, QING R · 2016 to 2018
$1.6M
NINDS NIH HHS R01 NS072427NINDS NIH HHS R01 NS075243NINDS NIH HHS R37 NS096359
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic and debilitating neurological disorder of the central nervous system (CNS), characterized by infiltration of leukocytes into CNS and subsequent demyelination. Emerging evidences have revealed the beneficial roles of M2 macrophages in ameliorating experimental autoimmune encephalomyelitis (EAE), a model for MS. Here, we identify that lenalidomide alone could promote macrophages M2 polarization to prevent the progression of EAE, which is associated with subsequent inhibition of proinflammatory Th1 and Th17 cells both in peripheral lymph system and CNS. Depletion of macrophages by pharmacology treatment of clodronate liposomes or transferring lenalidomide-induced BMDMs in EAE mice completely abolished the therapeutic effect of lenalidomide or prevented EAE development, respectively. The macrophages-derived IL10 was upregulated both in vivo and in vitro after lenalidomide treatment. Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10

Indexed as

AnimalsAutoimmunitybeta-N-AcetylhexosaminidasesCell CountCell DifferentiationCentral Nervous SystemClodronic AcidEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationImmunologic FactorsInterleukin-10LectinsLenalidomideLiposomesMacrophagesbeta-N-AcetylhexosaminidasesChil3 protein, mouseClodronic AcidIL10 protein, mouseImmunologic FactorsInterleukin-10LectinsLenalidomideLiposomesStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID29445144
PMCPMC5833426
OpenAlexW2789336169

What OpenQuestion holds

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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.