Evidence map›Paper›PMID 31354711›Full record

ArticleFrontiers in immunology2019

TLR7 Protein Expression in Mild and Severe Lupus-Prone Models Is Regulated in a Leukocyte, Genetic, and IRAK4 Dependent Manner.

Teja Celhar, Hao Kim Lu, Lia Benso, Larissa Rakhilina, Hui Yin Lee, Shubhita Tripathi, Olga Zharkova, Wei Yee Ong, Hiroko Yasuga, Bijin Au and 8 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Review
  9. Targeting the Myddosome in Systemic Autoimmunity: Ready for Prime Time?Arthritis & rheumatology (Hoboken, N.J.) · 2021
    Article
  10. Article
  11. Article
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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

18 authors at 8 institutions in 2 countries.

Teja CelharSingapore Immunology Network, ASTAR, Singapore, Singapore.
Hao Kim LuSingapore Immunology Network, ASTAR, Singapore, Singapore.
Lia BensoMerck & Co., Inc., Boston, MA, United States.
Larissa RakhilinaMerck & Co., Inc., Boston, MA, United States.
Hui Yin LeeSingapore Immunology Network, ASTAR, Singapore, Singapore.
Shubhita TripathiSingapore Immunology Network, ASTAR, Singapore, Singapore.
Olga ZharkovaSingapore Immunology Network, ASTAR, Singapore, Singapore.
Wei Yee OngInstitute of Molecular and Cell Biology, ASTAR, Singapore, Singapore.
Hiroko YasugaSingapore Immunology Network, ASTAR, Singapore, Singapore.
Bijin AuInstitute of Molecular and Cell Biology, ASTAR, Singapore, Singapore.
Damien MarlierTessa Therapeutics, Singapore, Singapore.
Lina Hsiu Kim LimDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Thomas Paulraj ThambooDepartment of Pathology, National University Hospital, Singapore, Singapore.
John S MudgettMerck & Co., Inc., Boston, MA, United States.
Matthew F MackeyMerck & Co., Inc., Boston, MA, United States.
Dennis M ZallerMerck & Co., Inc., Boston, MA, United States.
John E ConnollyInstitute of Molecular and Cell Biology, ASTAR, Singapore, Singapore.
Anna-Marie FairhurstSingapore Immunology Network, ASTAR, Singapore, Singapore.
Merck & Co., Inc., Rahway, NJ, USA (United States) · USAgency for Science, Technology and Research · SGInstitute of Molecular and Cell Biology · SGNanyang Technological University · SGSingapore Immunology Network · SGNational University Hospital · SGNational University of Singapore · SGTessa Therapeutic (Singapore) · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The global increase in autoimmunity, together with the emerging autoimmune-related side effects of cancer immunotherapy, have furthered a need for understanding of immune tolerance and activation. Systemic lupus erythematosus (SLE) is the archetypical autoimmune disease, affecting multiple organs, and tissues. Studying SLE creates knowledge relevant not just for autoimmunity, but the immune system in general. Murine models and patient studies have provided increasing evidence for the innate immune toll like receptor-7 (TLR7) in disease initiation and progression. Here, we demonstrated that the kinase activity of the TLR7-downstream signaling molecule, interleukin-1 receptor associated kinase 4 (IRAK4), is essential for mild and severe autoimmune traits of the

Indexed as

AnimalsAntibodies, AntinuclearCell MovementDendritic CellsDisease Models, AnimalGlomerulonephritisHumansImmunity, InnateInterleukin-1 Receptor-Associated KinasesKidneyLeukocytesLupus Erythematosus, SystemicLupus NephritisMacrophagesMiceMice, TransgenicAntibodies, AntinuclearInterleukin-1 Receptor-Associated KinasesIrak4 protein, mousePbx1 protein, mousePre-B-Cell Leukemia Transcription Factor 1Toll-Like Receptor 7anti-nuclear antibodydendritic cellsIRAK4lupusSLETLR7

Identifiers

PMID31354711
PMCPMC6636428
OpenAlexW2962408238

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.