Evidence map›Paper›PMID 23082204›Full record

ArticlePloS one2012

CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2.

Roy J Soberman, Christopher R MacKay, Christine A Vaine, Glennice Bowen Ryan, Anna M Cerny, Mikayla R Thompson, Boris Nikolic, Valeria Primo, Peter Christmas, Paul Sheiffele and 3 more

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. CD200 ModulatesInternational journal of molecular sciences · 2019
    Article
  10. Review
  11. Innate Immune Mechanisms and Herpes Simplex Virus Infection and Disease.Advances in anatomy, embryology, and cell biology · 2017
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
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

13 authors.

Roy J SobermanRenal Unit, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, USA. Soberman@helix.mgh.harvard.edu
Christopher R MacKay
Christine A Vaine
Glennice Bowen Ryan
Anna M Cerny
Mikayla R Thompson
Boris Nikolic
Valeria Primo
Peter Christmas
Paul Sheiffele
Lisa Aronov
David M Knipe
Evelyn A Kurt-Jones

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
UMASS MEDICAL CENTER FOR AIDS RESEARCHP30AI042845 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SOMASUNDARAN, MOHAN · 1998 to 2012
$13.0M
Innate Immunity and Herpes Simplex InfectionP01AI083215 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI FINBERG, ROBERT WILLIAM · 2009 to 2010
$3.7M
Leukotrienes and Lung InflammationR01AI068871 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI SOBERMAN, ROY · 2007 to 2011
$2.5M
Innate Immunity Training ProgramT32AI095213 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SILVERMAN, NEAL · 2011 to 2025
$2.5M
NIAID NIH HHS 5P30 AI-42845NIAID NIH HHS P01 AI083215NIAID NIH HHS P01 AI083215-01NIAID NIH HHS P30 AI042845NIAID NIH HHS R01 AI068871NIAID NIH HHS R01AI068871NIAID NIH HHS R01AI068871-S4NIAID NIH HHS T32 AI095213NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520
6 · The paper itself

Abstract

The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in regulating macrophage signaling via TLR2 as well as the host response to an in vivo, TLR2-dependent model, herpes simplex virus 1 (HSV-1) infection. CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in the generation of IL-6 and CCL5 (Rantes) in response to the TLR2 agonist Pam(2)CSK(4) and to HSV-1. CD200R1(-/-) macrophages could neither up-regulate the expression of TLR2, nor assemble a functional inflammasome in response to HSV-1. CD200R1(-/-) mice were protected from HSV-1 infection and exhibited dysfunctional TLR2 signaling. Finally, both CD200R1(-/-) mice and CD200R1(-/-) fibroblasts and macrophages showed a markedly reduced ability to support HSV-1 replication. In summary, our data demonstrate an unanticipated and novel requirement for CD200R1 in "licensing" pro-inflammatory functions of TLR2 and in limiting viral replication that are supported by ex vivo and in vivo evidence.

Indexed as

AnimalsAntigens, SurfaceBrainEmbryo, MammalianEncephalitisFibroblastsGene TargetingHerpesvirus 1, HumanInflammationInterferon Type IMacrophages, PeritonealMiceOrexin ReceptorsReceptors, Cell SurfaceSignal TransductionToll-Like Receptor 2Antigens, SurfaceCd200r1 protein, mouseInterferon Type IOrexin ReceptorsReceptors, Cell SurfaceTlr2 protein, mouseToll-Like Receptor 2

Identifiers

PMID23082204
PMCPMC3474780

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.