Evidence map›Paper›PMID 25229618›Full record

ArticlePloS one2014

Humanized TLR7/8 expression drives proliferative multisystemic histiocytosis in C57BL/6 mice.

Jessica M Snyder, Piper M Treuting, Lee Nagy, Cathy Yam, Jaehun Yi, Alicia Brasfield, Lisa Phuong Anh Nguyen, Adeline M Hajjar

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 15 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

8 authors at 1 institution in 1 country.

Jessica M SnyderDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America; Comparative Pathology Program, University of Washington, Seattle, Washington, United States of America.
Piper M TreutingDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America; Comparative Pathology Program, University of Washington, Seattle, Washington, United States of America.
Lee NagyDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
Cathy YamDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
Jaehun YiDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
Alicia BrasfieldDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
Lisa Phuong Anh NguyenDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
Adeline M HajjarDepartment of Comparative Medicine, University of Washington, Seattle, Washington, United States of America.
University of Washington · US

Funding

Laboratory Animal Medicine and Translational Research Training for VeterinariansR25OD010450 · OD · UNIVERSITY OF WASHINGTON · PI BRABB, THEA, IRITANI, BRIAN M · 2012 to 2015
$634k
NIAID NIH HHS HHSN272200900036CNIH HHS R25 OD010450NIH HHS R25 OD 010450-01A1
6 · The paper itself

Abstract

A humanized TLR7/TLR8 transgenic mouse line was engineered for studies using TLR7/8 ligands as vaccine adjuvants. The mice developed a spontaneous immune-mediated phenotype prior to six months of age characterized by runting, lethargy, blepharitis, and corneal ulceration. Histological examination revealed a marked, multisystemic histiocytic infiltrate that effaced normal architecture. The histological changes were distinct from those previously reported in mouse models of systemic lupus erythematosus. When the mice were crossed with MyD88-/- mice, which prevented toll-like receptor signaling, the inflammatory phenotype resolved. Illness may be caused by constitutive activation of human TLR7 or TLR8 in the bacterial artificial chromosome positive mice as increased TLR7 and TLR8 expression or activation has previously been implicated in autoimmune disease.

Indexed as

Gene ExpressionAnimalsCrosses, GeneticCytokinesDisease Models, AnimalFemaleGalectin 3Genetic LociGenotypeHistiocytosisHumansIntracellular SpaceMaleMiceMice, Inbred C57BLMice, KnockoutCytokinesGalectin 3Myeloid Differentiation Factor 88Toll-Like Receptor 7Toll-Like Receptor 8

Identifiers

PMID25229618
PMCPMC4168129
OpenAlexW1977284974

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.