Evidence map›Paper›PMID 19587008›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Murine B cell response to TLR7 ligands depends on an IFN-beta feedback loop.

Nathaniel M Green, Amy Laws, Kerstin Kiefer, Liliana Busconi, You-Me Kim, Melanie M Brinkmann, Erin Hodges Trail, Kei Yasuda, Sean R Christensen, Mark J Shlomchik and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

77 citing papers in PubMed, 120 citations in OpenAlex.

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17 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

17 authors at 6 institutions in 3 countries.

Nathaniel M GreenDepartment of Microbiology, Boston University School of Medicine, Boston, MA 02118, USA.
Amy Laws
Kerstin Kiefer
Liliana Busconi
You-Me Kim
Melanie M Brinkmann
Erin Hodges Trail
Kei Yasuda
Sean R Christensen
Mark J Shlomchik
Stefanie Vogel
John H Connor
Hidde Ploegh
Dan Eilat
Ian R Rifkin
Jean Maguire van Seventer
Ann Marshak-Rothstein
Czech Academy of Sciences, Institute of Microbiology · CZBoston University · USMassachusetts Institute of Technology · USYale University · USHadassah Academic College · ILUniversity of Maryland, Baltimore · US

Funding

Toll-Like Receptors in Systemic Autoimmune DiseaseP01AR050256 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHLOMCHIK, MARK J · 2004 to 2013
$13.4M
DIFFERENTIATIVE SIGNALS FOR MACROPHAGE ACTIVATIONR37AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2000 to 2009
$5.3M
DIFFERENTIATIVE SIGNALS FOR MACROPHANGE ACTIVATIONR01AI018797 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI VOGEL, STEFANIE N. · 1985 to 2014
$3.8M
B CELL HYPERACTIVITY IN AUTOIMMUNITYR01AR035230 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI MARSHAK-ROTHSTEIN, ANN · 1986 to 2010
$3.2M
Differentiative Signals for Macrophage ActivationR56AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2015 to 2015
$506k
NIAID NIH HHS AI18797NIAID NIH HHS R01 AI018797NIAID NIH HHS R37 AI018797NIAID NIH HHS R56 AI018797NIAMS NIH HHS AR35230NIAMS NIH HHS AR50256NIAMS NIH HHS P01 AR050256NIAMS NIH HHS R01 AR035230
6 · The paper itself

Abstract

Type I IFNs play an important, yet poorly characterized, role in systemic lupus erythematosus. To better understand the interplay between type I IFNs and the activation of autoreactive B cells, we evaluated the effect of type I IFN receptor (IFNAR) deficiency in murine B cell responses to common TLR ligands. In comparison to wild-type B cells, TLR7-stimulated IFNAR(-/-) B cells proliferated significantly less well and did not up-regulate costimulatory molecules. By contrast, IFNAR1(-/-) B cells did not produce cytokines, but did proliferate and up-regulate activation markers in response to other TLR ligands. These defects were not due to a difference in the distribution of B cell populations or a failure to produce a soluble factor other than a type I IFN. Instead, the compromised response pattern reflected the disruption of an IFN-beta feedback loop and constitutively low expression of TLR7 in the IFNAR1(-/-) B cells. These results highlight subtle differences in the IFN dependence of TLR7 responses compared with other TLR-mediated B cell responses.

Indexed as

AnimalsAutoimmunityB-LymphocytesCell ProliferationCytokinesFeedback, PhysiologicalInterferon-betaLigandsLymphocyte ActivationMiceMice, KnockoutReceptor, Interferon alpha-betaToll-Like Receptor 7CytokinesInterferon-betaLigandsReceptor, Interferon alpha-betaToll-Like Receptor 7

Identifiers

PMID19587008
PMCPMC2929820
OpenAlexW2132407227

What OpenQuestion holds

Textmetadata
LicenceTDM
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.