Evidence map›Paper›PMID 34591795›Full record

ArticleJCI insight2021

CD47 antibody blockade suppresses microglia-dependent phagocytosis and monocyte transition to macrophages, impairing recovery in EAE.

Huan Wang, Gail Newton, Liguo Wu, Lih-Ling Lin, Amy S Miracco, Sridaran Natesan, Francis W Luscinskas

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  7. Review
  8. Deciphering the role of CD47 in cancer immunotherapy.Journal of advanced research · 2024
    Review
  9. 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

7 authors at 2 institutions in 1 country.

Huan WangCenter for Excellence in Vascular Biology, Department of Pathology, Mass General Brigham and Harvard Medical School, Boston, Massachusetts, USA.
Gail NewtonCenter for Excellence in Vascular Biology, Department of Pathology, Mass General Brigham and Harvard Medical School, Boston, Massachusetts, USA.
Liguo WuImmunology & Inflammation Research Therapeutic Area, Sanofi US, Cambridge, Massachusetts, USA.
Lih-Ling LinImmunology & Inflammation Research Therapeutic Area, Sanofi US, Cambridge, Massachusetts, USA.
Amy S MiraccoImmunology & Inflammation Research Therapeutic Area, Sanofi US, Cambridge, Massachusetts, USA.
Sridaran NatesanImmunology & Inflammation Research Therapeutic Area, Sanofi US, Cambridge, Massachusetts, USA.
Francis W LuscinskasCenter for Excellence in Vascular Biology, Department of Pathology, Mass General Brigham and Harvard Medical School, Boston, Massachusetts, USA.
Inflammation Research Foundation · USCenter for Systems Biology · US

Funding

CD47 Regulation of Leukocyte Integrins during Leukocyte TraffickingR01HL125780 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LUSCINSKAS, FRANCIS W. · 2016 to 2019
$2.3M
NHLBI NIH HHS R01 HL125780
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a well-characterized animal model of multiple sclerosis. During the early phase of EAE, infiltrating monocytes and monocyte-derived macrophages contribute to T cell recruitment, especially CD4+ T cells, into the CNS, resulting in neuronal demyelination; however, in later stages, they promote remyelination and recovery by removal of myelin debris by phagocytosis. Signal regulatory protein α and CD47 are abundantly expressed in the CNS, and deletion of either molecule is protective in myelin oligodendrocyte glycoprotein-induced EAE because of failed effector T cell expansion and trafficking. Here we report that treatment with the function blocking CD47 Ab Miap410 substantially reduced the infiltration of pathogenic immune cells but impaired recovery from paresis. The underlying mechanism was by blocking the emergence of CD11chiMHCIIhi microglia at peak disease that expressed receptors for phagocytosis, scavenging, and lipid catabolism, which mediated clearance of myelin debris and the transition of monocytes to macrophages in the CNS. In the recovery phase of EAE, Miap410 Ab-treated mice had worsening paresis with sustained inflammation and limited remyelination as compared with control Ab-treated mice. In summary, Ab blockade of CD47 impaired resolution of CNS inflammation, thus worsening EAE.

Indexed as

AnimalsCD47 AntigenDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleMacrophagesMiceMice, KnockoutMicrogliaMonocytesPhagocytosisCD47 AntigenAutoimmune diseasesInflammation

Identifiers

PMID34591795
PMCPMC8663579
OpenAlexW3204576894

What OpenQuestion holds

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LicenceCC BY
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.