Evidence map›Paper›PMID 14742268›Full record

ArticleThe American journal of pathology2004

CXCR3 is involved in tubulointerstitial injury in human glomerulonephritis.

Stephan Segerer, Bernhard Banas, Markus Wörnle, Holger Schmid, Clemens D Cohen, Matthias Kretzler, Matthias Mack, Eva Kiss, Peter J Nelson, Detlef Schlöndorff and 1 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.5field-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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
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  12. Human Extrafollicular CD4Journal of immunology (Baltimore, Md. : 1950) · 2018
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  17. CXCR3+ Regulatory T Cells Control TH1 Responses in Crescentic GN.Journal of the American Society of Nephrology : JASN · 2016
    Article
  18. Serum TWEAK as a biomarker for disease activity of systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    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

11 authors at 4 institutions in 1 country.

Stephan SegererMedizinische Poliklinik-Innenstadt, University of Munich, Munich, Germany. Stephan.segerer@lrz.uni-muenchen.de
Bernhard Banas
Markus Wörnle
Holger Schmid
Clemens D Cohen
Matthias Kretzler
Matthias Mack
Eva Kiss
Peter J Nelson
Detlef Schlöndorff
Hermann-Josef Gröne
Klinik und Poliklinik für Orthopädie, Physikalische Medizin und Rehabilitation · DEUniversity of Regensburg · DEGerman Cancer Research Center · DELMU Klinikum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokines play pivotal roles in the recruitment of inflammatory cells into the kidney. The chemokine receptors CXCR3 and CCR5 are expressed on activated T lymphocytes, and expression of CXCR3 by mesangial cells has been suggested. Detailed description of CXCR3 expression might form a rational basis for use as a diagnostic marker and for therapeutic CXCR3 targeting in human glomerulonephritis. We studied the expression of CXCR3 in renal biopsies by immunohistochemistry (n = 45), and real time RT-PCR (n = 78). Biopsies were from patients with IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis. Furthermore, cultured human mesangial cells (HMC) were studied for CXCR3 expression, and for functional responses to the ligands CXCL10/IP-10 and CXCL9/Mig. CXCR3-positive cells were rarely found in glomerular tufts, but formed a major part of the tubulointerstitial infiltrates. Consistently, CXCR3 mRNA expression was too low to be quantified in glomerular compartments, and was not detectable in HMC. The published staining for CXCR3 of mesangial cells could be traced to cross-reactivity of an antibody for CXCR3 with a potentially related chemokine receptor as revealed by FACS analysis. Despite an absence of CXCR3 expression, mesangial cells reacted to CXCR3 ligands by proliferation and migration, which was blocked by pertussis toxin but not by an anti-CXCR3 antibody. These results indicate that HMC do not express the classical CXCR3, but may potentially express a related receptor with shared ligand specificity. By immunohistochemistry the number of CXCR3-positive cells, mainly interstitial T cells, correlated with renal function, proteinuria, and percentage of globally sclerosed glomeruli. A significant morphological and numerical correlation between CD3, CXCR3, and CCR5-positive cells indicated a CXCR3/CCR5 double-positive T cell population. No apparent difference in the CXCR3 expression pattern was found between disease entities. CXCR3 expression was localized to interstitial T cells, and these cells correlated strongly with important prognostic markers. Therefore interstitial CXCR3, as well as CCR5-positive T cells might play an important role during progressive loss of renal function, and are potential therapeutic targets in human glomerular diseases.

Indexed as

AdolescentAdultBase SequenceBiopsyCells, CulturedChemokine CXCL10Chemokine CXCL9Chemokines, CXCChemotaxisFemaleFlow CytometryGlomerular MesangiumGlomerulonephritisHumansImmunohistochemistryIntercellular Signaling Peptides and ProteinsChemokine CXCL10Chemokine CXCL9Chemokines, CXCCXCL9 protein, humanCXCR3 protein, humanIntercellular Signaling Peptides and ProteinsReceptors, CCR5Receptors, ChemokineReceptors, CXCR3

Identifiers

PMID14742268
PMCPMC1602271
OpenAlexW2072898308

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.