Evidence map›Paper›PMID 23999431›Full record

ArticleThe Journal of clinical investigation2013

Exclusive CX3CR1 dependence of kidney DCs impacts glomerulonephritis progression.

Katharina Hochheiser, Christoph Heuser, Torsten A Krause, Simon Teteris, Anissa Ilias, Christina Weisheit, Florian Hoss, André P Tittel, Percy A Knolle, Ulf Panzer and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 92 citations in OpenAlex.

  1. Observational
  2. Myeloid Cells in Acute Kidney Injury.Seminars in nephrology · 2025
    Review
  3. Review
  4. Article
  5. CXInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  6. Article
  7. Frontiers in immunology · 2023
    Article
  8. Article
  9. Immunosenescence: an unexplored role in glomerulonephritis.Clinical & translational immunology · 2022
    Review
  10. Article
  11. Review
  12. Review
  13. Role of Dendritic Cell in Diabetic Nephropathy.International journal of molecular sciences · 2021
    Review
  14. Renal CD169Life science alliance · 2021
    Article
  15. Novel Risk Factors for Progression of Diabetic and Nondiabetic CKD: Findings From the Chronic Renal Insufficiency Cohort (CRIC) Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2021
    Observational
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

13 authors at 1 institution in 1 country.

Katharina Hochheiser
Christoph Heuser
Torsten A Krause
Simon Teteris
Anissa Ilias
Christina Weisheit
Florian Hoss
André P Tittel
Percy A Knolle
Ulf Panzer
Daniel R Engel
Pierre-Louis Tharaux
Christian Kurts
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DCs and macrophages both express the chemokine receptor CX3CR1. Here we demonstrate that its ligand, CX3CL1, is highly expressed in the murine kidney and intestine. CX3CR1 deficiency markedly reduced DC numbers in the healthy and inflamed kidney cortex, and to a lesser degree in the kidney medulla and intestine, but not in other organs. CX3CR1 also promoted influx of DC precursors in crescentic glomerulonephritis, a DC-dependent aggressive type of nephritis. Disease severity was strongly attenuated in CX3CR1-deficient mice. Primarily CX3CR1-dependent DCs in the kidney cortex processed antigen for the intrarenal stimulation of T helper cells, a function important for glomerulonephritis progression. In contrast, medullary DCs played a specialized role in inducing innate immunity against bacterial pyelonephritis by recruiting neutrophils through rapid chemokine production. CX3CR1 deficiency had little effect on the immune defense against pyelonephritis, as medullary DCs were less CX3CR1 dependent than cortical DCs and because recruited neutrophils produced chemokines to compensate for the DC paucity. These findings demonstrate that cortical and medullary DCs play specialized roles in their respective kidney compartments. We identify CX3CR1 as a potential therapeutic target in glomerulonephritis that may involve fewer adverse side effects, such as impaired anti-infectious defense or compromised DC functions in other organs.

Indexed as

AnimalsAntigen PresentationCells, CulturedCX3C Chemokine Receptor 1Dendritic CellsDisease ProgressionFemaleGlomerulonephritisHistocompatibility Antigens Class IIImmunity, InnateKidneyMacrophagesMiceMice, Inbred C57BLMice, TransgenicPyelonephritisCX3C Chemokine Receptor 1Cx3cr1 protein, mouseHistocompatibility Antigens Class IIReceptors, Chemokine

Identifiers

PMID23999431
PMCPMC3784547
OpenAlexW2136984446

What OpenQuestion holds

Textmetadata
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.