Evidence map›Paper›PMID 18779347›Full record

ArticleThe Journal of experimental medicine2008

Ly6c+ "inflammatory monocytes" are microglial precursors recruited in a pathogenic manner in West Nile virus encephalitis.

Daniel R Getts, Rachael L Terry, Meghann Teague Getts, Marcus Müller, Sabita Rana, Bimmi Shrestha, Jane Radford, Nico Van Rooijen, Iain L Campbell, Nicholas J C King

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
231citing papers in PubMed, 2 pooled it
14.2field-weighted citation impact, top 1% 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

231 citing papers in PubMed, 2 syntheses or guidelines pooled it, 366 citations in OpenAlex.

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  15. Metabolic Programming Drives Protective and Inflammatory Monocyte Fates in Viral Encephalitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  19. Review
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171 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

10 authors at 1 institution in 2 countries.

Daniel R GettsThe Discipline of Pathology, School of Medical Sciences, The University of Sydney, Sydney NSW 2006, Australia.
Rachael L Terry
Meghann Teague Getts
Marcus Müller
Sabita Rana
Bimmi Shrestha
Jane Radford
Nico Van Rooijen
Iain L Campbell
Nicholas J C King
University of Sydney · AU

Funding

Interleukin 12 in inflammatory neurological diseasesR01NS036979 · NINDS · UNIVERSITY OF SYDNEY · PI CAMPBELL, IAIN LESLIE · 1998 to 2007
$2.1M
CNS Pathobiology of IFN-inducible non-ELR CXC ChemokinesR01NS044905 · NINDS · UNIVERSITY OF SYDNEY · PI CAMPBELL, IAIN LESLIE · 2004 to 2008
$1.2M
NINDS NIH HHS NS036979NINDS NIH HHS NS044905NINDS NIH HHS R01 NS036979NINDS NIH HHS R01 NS044905
6 · The paper itself

Abstract

In a lethal West Nile virus (WNV) model, central nervous system infection triggered a threefold increase in CD45(int)/CD11b(+)/CD11c(-) microglia at days 6-7 postinfection (p.i.). Few microglia were proliferating, suggesting that the increased numbers were derived from a migratory precursor cell. Depletion of "circulating" (Gr1(-)(Ly6C(lo))CX3CR1(+)) and "inflammatory" (Gr1(hi)/Ly6C(hi)/CCR2(+)) classical monocytes during infection abrogated the increase in microglia. C57BL/6 chimeras reconstituted with cFMS-enhanced green fluorescent protein (EGFP) bone marrow (BM) showed large numbers of peripherally derived (GFP(+)) microglia expressing GR1(+)(Ly6C(+)) at day 7 p.i., suggesting that the inflammatory monocyte is a microglial precursor. This was confirmed by adoptive transfer of labeled BM (Ly6C(hi)/CD115(+)) or circulating inflammatory monocytes that trafficked to the WNV-infected brain and expressed a microglial phenotype. CCL2 is a chemokine that is highly expressed during WNV infection and important in inflammatory monocyte trafficking. Neutralization of CCL2 not only reduced the number of GFP(+) microglia in the brain during WNV infection but prolonged the life of infected animals. Therefore, CCL2-dependent inflammatory monocyte migration is critical for increases in microglia during WNV infection and may also play a pathogenic role during WNV encephalitis.

Indexed as

Adoptive TransferAnimalsAntigens, LyBlood-Brain BarrierBrainChemokine CCL2Clodronic AcidFemaleLeukocyte Common AntigensLiposomesMiceMice, Inbred C57BLMicrogliaMonocytesStem CellsSurvival RateAntigens, LyCcl2 protein, mouseChemokine CCL2Clodronic AcidLeukocyte Common AntigensLiposomesLy-6C antigen, mousePtprc protein, mouse

Identifiers

PMID18779347
PMCPMC2556789
OpenAlexW2102947626

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.