Evidence map›Paper›PMID 34868046›Full record

ArticleFrontiers in immunology2021

Anti-TLR7 Antibody Protects Against Lupus Nephritis in NZBWF1 Mice by Targeting B Cells and Patrolling Monocytes.

Yusuke Murakami, Ryutaro Fukui, Reika Tanaka, Yuji Motoi, Atsuo Kanno, Ryota Sato, Kiyoshi Yamaguchi, Hirofumi Amano, Yoichi Furukawa, Hitoshi Suzuki and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 42 citations in OpenAlex.

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  18. Endosomal Toll-Like Receptors as Therapeutic Targets for Autoimmune Diseases.Advances in experimental medicine and biology · 2024
    Article
  19. TLR7/8 stress response drives histiocytosis in SLC29A3 disorders.The Journal of experimental medicine · 2023
    Article
  20. EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023
    Article
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

14 authors at 3 institutions in 1 country.

Yusuke MurakamiDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ryutaro FukuiDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Reika TanakaDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yuji MotoiDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Atsuo KannoDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ryota SatoDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Kiyoshi YamaguchiDivision of Clinical Genome Research, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hirofumi AmanoDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Yoichi FurukawaDivision of Clinical Genome Research, Advanced Clinical Research Center, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Hitoshi SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Yusuke SuzukiDepartment of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Naoto TamuraDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Naomi YamashitaFaculty of Pharmacy, Department of Pharmaceutical Sciences & Research Institute of Pharmaceutical Sciences, Musashino University, Tokyo, Japan.
Kensuke MiyakeDivision of Innate Immunity, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
The University of Tokyo · JPJuntendo University · JPMusashino University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and multiple organ damage. Toll-like receptor 7 (TLR7), an innate immune RNA sensor expressed in monocytes/macrophages, dendritic cells (DCs), and B cells, promotes disease progression. However, little is known about the cellular mechanisms through which TLR7 drives lupus nephritis. Here, we show that the anti-mouse TLR7 mAb, but not anti-TLR9 mAb, protected lupus-prone NZBWF1 mice from nephritis. The anti-TLR7 mAb reduced IgG deposition in glomeruli by inhibiting the production of autoantibodies to the RNA-associated antigens. We found a disease-associated increase in Ly6C

Indexed as

AnimalsAutoantibodiesAutoantigensAutoimmunityBiomarkersB-LymphocytesDisease Models, AnimalDisease SusceptibilityGene Expression RegulationImmunoglobulin GImmunohistochemistryImmunophenotypingLupus NephritisMiceMonocytesToll-Like Receptor 7AutoantibodiesAutoantigensBiomarkersImmunoglobulin GToll-Like Receptor 7autoantibodyinhibitory monoclonal antibodylupus nephritismonocytestoll-like receptor

Identifiers

PMID34868046
PMCPMC8632649
OpenAlexW3214026160

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.