Evidence map›Paper›PMID 27137488›Full record

ArticleEMBO molecular medicine2016

Interferon-beta signaling in retinal mononuclear phagocytes attenuates pathological neovascularization.

Anika Lückoff, Albert Caramoy, Rebecca Scholz, Marco Prinz, Ulrich Kalinke, Thomas Langmann

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
6.0field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Interferon-mediated regulation of the neurovascular unit in diabetic retinopathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  18. Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Anika LückoffRetinal Immunology Laboratory (RIL), Department of Ophthalmology, University of Cologne, Cologne, Germany.
Albert CaramoyRetinal Immunology Laboratory (RIL), Department of Ophthalmology, University of Cologne, Cologne, Germany.
Rebecca ScholzRetinal Immunology Laboratory (RIL), Department of Ophthalmology, University of Cologne, Cologne, Germany.
Marco PrinzInstitute of Neuropathology and BIOSS Center for Biological Signaling Studies, University of Freiburg, Freiburg, Germany.
Ulrich KalinkeInstitute for Experimental Infection Research, TWINCORE Centre for Experimental and Clinical Infection Research a joint venture between the Helmholtz Centre for Infection Research and the Hannover Medical School, Hannover, Germany.
Thomas LangmannRetinal Immunology Laboratory (RIL), Department of Ophthalmology, University of Cologne, Cologne, Germany thomas.langmann@uk-koeln.de.ORCID 0000-0001-6826-529X
University of Cologne · DEMedizinische Hochschule Hannover · DEUniversity of Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD) is a leading cause of vision loss among the elderly. AMD pathogenesis involves chronic activation of the innate immune system including complement factors and microglia/macrophage reactivity in the retina. Here, we show that lack of interferon-β signaling in the retina accelerates mononuclear phagocyte reactivity and promotes choroidal neovascularization (CNV) in the laser model of neovascular AMD Complete deletion of interferon-α/β receptor (Ifnar) using Ifnar1(-/-) mice significantly enhanced early microglia and macrophage activation in lesion areas. This triggered subsequent vascular leakage and CNV at later stages. Similar findings were obtained in laser-treated Cx3cr1(Cre) (ER):Ifnar1(fl/fl) animals that allowed the tamoxifen-induced conditional depletion of Ifnar in resident mononuclear phagocytes only. Conversely, systemic IFN-β therapy of laser-treated wild-type animals effectively attenuated microgliosis and macrophage responses in the early stage of disease and significantly reduced CNV size in the late phase. Our results reveal a protective role of Ifnar signaling in retinal immune homeostasis and highlight a potential use for IFN-β therapy in the eye to limit chronic inflammation and pathological angiogenesis in AMD.

Indexed as

Neovascularization, PathologicSignal TransductionAnimalsDisease Models, AnimalInterferon-betaMacrophage ActivationMacular DegenerationMiceMice, KnockoutPhagocytesRetinaInterferon-betaage‐related macular degenerationchoroidal neovascularizationinterferon‐beta signalingmacrophagesmicroglia

Identifiers

PMID27137488
PMCPMC4888856
OpenAlexW2345436298

What OpenQuestion holds

Textmetadata
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.