Evidence map›Paper›PMID 30107066›Full record

ArticleImmunology and cell biology2019

Constitutive overexpression of TNF in BPSM1 mice causes iBALT and bone marrow nodular lymphocytic hyperplasia.

Cyril Seillet, Elyas H Arvell, Derek Lacey, Michael D Stutz, Marc Pellegrini, Lachlan Whitehead, Joel Rimes, Edwin D Hawkins, Ben Roediger, Gabrielle T Belz and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunology and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

11 authors at 3 institutions in 1 country.

Cyril SeilletThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Elyas H ArvellThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Derek LaceyThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Michael D StutzThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Marc PellegriniThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Lachlan WhiteheadThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Joel RimesThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Edwin D HawkinsThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Ben RoedigerThe Centenary Institute, Camperdown, NSW, 2050, Australia.
Gabrielle T BelzThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
Philippe BouilletThe Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, 3052, Australia.
University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AUCentenary Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BPSM1 (Bone phenotype spontaneous mutant 1) mice develop severe polyarthritis and heart valve disease as a result of a spontaneous mutation in the Tnf gene. In these mice, the insertion of a retrotransposon in the 3' untranslated region of Tnf causes a large increase in the expression of the cytokine. We have found that these mice also develop inducible bronchus-associated lymphoid tissue (iBALT), as well as nodular lymphoid hyperplasia (NLH) in the bone marrow. Loss of TNFR1 prevents the development of both types of follicles, but deficiency of TNFR1 in the hematopoietic compartment only prevents the iBALT and not the NLH phenotype. We show that the development of arthritis and heart valve disease does not depend on the presence of the tertiary lymphoid tissues. Interestingly, while loss of IL-17 or IL-23 limits iBALT and NLH development to some extent, it has no effect on polyarthritis or heart valve disease in BPSM1 mice.

Indexed as

AnimalsBone MarrowHyperplasiaInterleukin-17Interleukin-23Lymphoid TissueMiceReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaIl17a protein, mouseInterleukin-17Interleukin-23Receptors, Tumor Necrosis FactorTnf protein, mouseTnfrsf23 protein, mouseTumor Necrosis Factor-alphaArthritisBPSM1heart valve diseaseiBALTIL-17IL-23NLHnodular lymphoid hyperplasiatertiary lymphoid organs, bronchus-associatedTNF

Identifiers

PMID30107066
PMCPMC6378607
OpenAlexW2885579062

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.