Evidence map›Paper›PMID 29408905›Full record

ArticlePloS one2018

Splenic macrophages are required for protective innate immunity against West Nile virus.

Marianne A Bryan, Daniela Giordano, Kevin E Draves, Richard Green, Michael Gale, Edward A Clark

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Marianne A BryanDepartment of Immunology, University of Washington, Seattle, WA, United States of America.
Daniela GiordanoDepartment of Immunology, University of Washington, Seattle, WA, United States of America.
Kevin E DravesDepartment of Immunology, University of Washington, Seattle, WA, United States of America.
Richard GreenDepartment of Immunology, University of Washington, Seattle, WA, United States of America.
Michael GaleDepartment of Immunology, University of Washington, Seattle, WA, United States of America.
Edward A ClarkDepartment of Immunology, University of Washington, Seattle, WA, United States of America.ORCID 0000-0001-8061-5475
University of Washington · US

Funding

Washington National Primate Research CenterP51OD010425 · OD · UNIVERSITY OF WASHINGTON · PI Mari Ostendorf · 2012 to 2026
$201.8M
Unlocking Zika Virus Immune Control and Pathogenesis with the Collaborative CrossU19AI100625 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HEISE, MARK T · 2012 to 2021
$36.6M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
Programming protective immunity by targeting antigens to the CD180 receptorR01AI052203 · NIAID · UNIVERSITY OF WASHINGTON · PI FULLER, DEBORAH H. · 2003 to 2019
$6.3M
Innate Immune Control of West Nile VirusR01AI104002 · NIAID · UNIVERSITY OF WASHINGTON · PI DIAMOND, MICHAEL S, GALE, MICHAEL · 2013 to 2017
$3.7M
NIAID NIH HHS R01 AI052203NIAID NIH HHS R01 AI104002NIAID NIH HHS U19 AI083019NIAID NIH HHS U19 AI100625NIH HHS P51 OD010425NIH HHS R01 AI52203NIH HHS RO1 AI104002
6 · The paper itself

Abstract

Although the spleen is a major site for West Nile virus (WNV) replication and spread, relatively little is known about which innate cells in the spleen replicate WNV, control viral dissemination, and/or prime innate and adaptive immune responses. Here we tested if splenic macrophages (MΦs) were necessary for control of WNV infection. We selectively depleted splenic MΦs, but not draining lymph node MΦs, by injecting mice intravenously with clodronate liposomes several days prior to infecting them with WNV. Mice missing splenic MΦs succumbed to WNV infection after an increased and accelerated spread of virus to the spleen and the brain. WNV-specific Ab and CTL responses were normal in splenic MΦ-depleted mice; however, numbers of NK cells and CD4 and CD8 T cells were significantly increased in the brains of infected mice. Splenic MΦ deficiency led to increased WNV in other splenic innate immune cells including CD11b- DCs, newly formed MΦs and monocytes. Unlike other splenic myeloid subsets, splenic MΦs express high levels of mRNAs encoding the complement protein C1q, the apoptotic cell clearance protein Mertk, the IL-18 cytokine and the FcγR1 receptor. Splenic MΦ-deficient mice may be highly susceptible to WNV infection in part to a deficiency in C1q, Mertk, IL-18 or Caspase 12 expression.

Indexed as

Immunity, InnateAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesFemaleMacrophagesMaleMiceMice, Inbred C57BLSpleenT-Lymphocytes, CytotoxicViral LoadWest Nile virus

Identifiers

PMID29408905
PMCPMC5800658
OpenAlexW2789486695

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.