Evidence map›Paper›PMID 21084753›Full record

ArticleThe Journal of clinical investigation2010

The proteoglycan biglycan regulates expression of the B cell chemoattractant CXCL13 and aggravates murine lupus nephritis.

Kristin Moreth, Rebekka Brodbeck, Andrea Babelova, Norbert Gretz, Tilmann Spieker, Jinyang Zeng-Brouwers, Josef Pfeilschifter, Marian F Young, Roland M Schaefer, Liliana Schaefer

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In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

126 citing papers in PubMed, 205 citations in OpenAlex.

  1. Article
  2. Article
  3. [Regulatory effects of mesenchymal stem cells on B1 cells and Tfh cells in children with systemic lupus erythematosus].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  4. Article
  5. Article
  6. Review
  7. Sulfated Glycosaminoglycans in Inflammation.Advances in experimental medicine and biology · 2026
    Review
  8. Article
  9. Cxcl9Communications biology · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

66 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Kristin Moreth1Pharmazentrum Frankfurt, Institut für Allgemeine Pharmakologie und Toxikologie/ZAFES, Klinikum der JW Goethe-Universität Frankfurt am Main, Frankfurt am Main, Germany.
Rebekka Brodbeck
Andrea Babelova
Norbert Gretz
Tilmann Spieker
Jinyang Zeng-Brouwers
Josef Pfeilschifter
Marian F Young
Roland M Schaefer
Liliana Schaefer
University of Münster · DEHeidelberg University · DE

Funding

Function Of Skeletal Matrix GenesZIADE000379 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI YOUNG, MARIAN F · 2009 to 2023
$23.6M
Intramural NIH HHS
6 · The paper itself

Abstract

CXCL13 is a key B cell chemoattractant and marker of disease activity in patients with SLE; however, the mechanism of its induction has not been identified yet. Here, we have shown that the proteoglycan biglycan triggers CXCL13 expression via TLR2/4 in macrophages and dendritic cells. In vivo, levels of biglycan were markedly elevated in the plasma and kidneys of human SLE patients and lupus-prone (MRL/lpr) mice. Overexpression of soluble biglycan in MRL/lpr mice raised plasma and renal levels of CXCL13 and caused accumulation of B cells with an enhanced B1/B cell ratio in the kidney, worsening of organ damage, and albuminuria. Importantly, biglycan also triggered CXCL13 expression and B cell infiltration in the healthy kidney. Conversely, biglycan deficiency improved systemic and renal outcome in lupus-prone mice, with lower levels of autoantibodies, less enlargement of the spleen and lymph nodes, and reduction in renal damage and albuminuria. This correlated with a marked decline in circulating and renal CXCL13 and a reduction in the number of B cells in the kidney. Collectively, our results describe what we believe to be a novel mechanism for the regulation of CXCL13 by biglycan, a host-derived ligand for TLR2/4. Blocking biglycan-TLR2/4 interactions might be a promising strategy for the management of SLE and other B cell-mediated inflammatory disease entities.

Indexed as

AdolescentAdultAnimalsBiglycanB-LymphocytesCase-Control StudiesChemokine CXCL13ChemokinesCytokinesDiabetic NephropathiesFemaleGraft RejectionHumansKidneyLupus Erythematosus, SystemicLupus NephritisBGN protein, humanBgn protein, mouseBiglycanChemokine CXCL13ChemokinesCXCL13 protein, humanCxcl13 protein, mouseCytokinesTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID21084753
PMCPMC2993585
OpenAlexW1968712129

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.