Evidence map›Paper›PMID 34518373›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

Selective depletion of a CD64-expressing phagocyte subset mediates protection against toxic kidney injury and failure.

Natallia Salei, Xingqi Ji, Dalia Pakalniškytė, Vanessa Kuentzel, Stephan Rambichler, Na Li, Markus Moser, Katja Steiger, Thorsten Buch, Hans-Joachim Anders and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
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  3. Review
  4. ANKRD22 promotes resolution of psoriasiform skin inflammation by antagonizing NIK-mediated IL-23 production.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  5. Article
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  8. Review
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 5 institutions in 3 countries.

Natallia SaleiWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany.
Xingqi JiWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany.
Dalia PakalniškytėWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany.ORCID 0000-0003-1717-7307
Vanessa KuentzelWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany.
Stephan RambichlerWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany.
Na LiDivision of Nephrology, The Seventh Affiliated Hospital, Sun Yat-sen University, 518107 Shenzhen, China.ORCID 0000-0002-4059-4507
Markus MoserInstitute of Experimental Hematology, School of Medicine, Technische Universität München, D-81675 Munich, Germany.
Katja SteigerInstitute of Pathology, School of Medicine, Technische Universität München, D-81675 München, Germany.ORCID 0000-0002-7269-5433
Thorsten BuchInstitute of Laboratory Animal Science, University of Zürich, 8956 Zürich, Switzerland.ORCID 0000-0002-2236-9074
Hans-Joachim AndersDivision of Nephrology, Medizinische Klinik und Poliklinik IV, University Hospital, Ludwig-Maximilians-Universität in Munich, 80366 Munich, Germany.
Barbara U SchramlWalter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität in Munich, 82152 Planegg-Martinsried, Germany; Barbara.schraml@bmc.med.lmu.de.ORCID 0000-0002-5801-0151
Ludwig-Maximilians-Universität München · DETechnical University of Munich · DELMU Klinikum · DESun Yat-sen University · CNUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DC), macrophages, and monocytes, collectively known as mononuclear phagocytes (MPs), critically control tissue homeostasis and immune defense. However, there is a paucity of models allowing to selectively manipulate subsets of these cells in specific tissues. The steady-state adult kidney contains four MP subsets with Clec9a-expression history that include the main conventional DC1 (cDC1) and cDC2 subtypes as well as two subsets marked by CD64 but varying levels of F4/80. How each of these MP subsets contributes to the different phases of acute kidney injury and repair is unknown. We created a mouse model with a Cre-inducible lox-STOP-lox-diphtheria toxin receptor cassette under control of the endogenous CD64 locus that allows for diphtheria toxin-mediated depletion of CD64-expressing MPs without affecting cDC1, cDC2, or other leukocytes in the kidney. Combined with specific depletion of cDC1 and cDC2, we revisited the role of MPs in cisplatin-induced kidney injury. We found that the intrinsic potency reported for CD11c

Indexed as

Acute Kidney InjuryAnimalsAntineoplastic AgentsCisplatinDendritic CellsFemaleHeparin-binding EGF-like Growth FactorMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMonocytesPhagocytesReceptors, IgGAntineoplastic AgentsCisplatinHeparin-binding EGF-like Growth FactorReceptors, IgGacute kidney injurycisplatindendritic cellsmacrophagesnecroinflammation

Identifiers

PMID34518373
PMCPMC8488624
OpenAlexW3200213969

What Socratic 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 Socratic graph.