Evidence map›Paper›PMID 14617752›Full record

Trial reportThe Journal of clinical investigation2003

Abnormal germinal center reactions in systemic lupus erythematosus demonstrated by blockade of CD154-CD40 interactions.

Amrie C Grammer, Rebecca Slota, Randy Fischer, Hanan Gur, Hermann Girschick, Cheryl Yarboro, Gabor G Illei, Peter E Lipsky

Erratum issuedOpen access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

101 citing papers in PubMed, 230 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Vitamin D decreases CD40L gene expression in ulcerative colitis patients: A randomized, double-blinded, placebo-controlled trial.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020
    Trial
  4. Failure of B Cell Tolerance in CVID.Frontiers in immunology · 2019
    Trial
  5. Trial
  6. Trial
  7. Germinal center responses at barrier organ sites.Current opinion in immunology · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Targeting B Cells and Plasma Cells in Glomerular Disease.Journal of the American Society of Nephrology : JASN · 2025
    Review
  12. Review
  13. Review
  14. Review
  15. Frontiers in immunology · 2024
    Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. B Cell Aberrance in Lupus: the Ringleader and the Solution.Clinical reviews in allergy & immunology · 2022
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Amrie C GrammerAutoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland 20892, USA. grammera@mail.nih.gov
Rebecca Slota
Randy Fischer
Hanan Gur
Hermann Girschick
Cheryl Yarboro
Gabor G Illei
Peter E Lipsky
Autoimmune Technologies (United States) · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USOffice of the Director · US

Funding

B CELL SIGNALLINGZ01AR041128 · NIAMS · ARTHRITIS, MUSCULOSKELETAL, SKIN DIS · PI LIPSKY, PETER E · 2000 to 2007
$1.1M
STUDIES OF THE PATHOGENESIS, NATURAL HISTORY &TREATMENT OF LUPUS NEPHRITISZ01AR041121 · NIAMS · ARTHRITIS, MUSCULOSKELETAL, SKIN DIS · PI LIPSKY, PETER E · 1998 to 2006
–
6 · The paper itself

Abstract

To determine the role of CD154-CD40 interactions in the B cell overactivity exhibited by patients with active systemic lupus erythematosus (SLE), CD19+ peripheral B cells were examined before and after treatment with humanized anti-CD154 mAb (BG9588, 5c8). Before treatment, SLE patients manifested activated B cells that expressed CD154, CD69, CD38, CD5, and CD27. Cells expressing CD38, CD5, or CD27 disappeared from the periphery during treatment with anti-CD154 mAb, and cells expressing CD69 and CD154 disappeared from the periphery during the post-treatment period. Before treatment, active-SLE patients had circulating CD38 (bright) Ig-secreting cells that were not found in normal individuals. Disappearance of this plasma cell subset during treatment was associated with decreases in anti-double-stranded DNA (anti-dsDNA) Ab levels, proteinuria, and SLE disease activity index. Consistent with this finding, peripheral B cells cultured in vitro spontaneously proliferated and secreted Ig in a manner that was inhibited by anti-CD154 mAb. Finally, the CD38(+/++)IgD(+), CD38(+++), and CD38(+)IgD(-) B cell subsets present in the peripheral blood also disappeared following treatment with humanized anti-CD154. Together, these results indicate that patients with active lupus nephritis exhibit abnormalities in the peripheral B cell compartment that are consistent with intensive germinal center activity, are driven via CD154-CD40 interactions, and may reflect or contribute to the propensity of these patients to produce autoantibodies.

Indexed as

AdultAnimalsAntibodies, MonoclonalBiomarkersB-Lymphocyte SubsetsCD40 AntigensCD40 LigandCD4-Positive T-LymphocytesCells, CulturedFemaleGerminal CenterHumansLupus Erythematosus, SystemicMicePhenotypeAntibodies, MonoclonalBiomarkersCD40 AntigensCD40 Ligand

Identifiers

PMID14617752
PMCPMC259134
OpenAlexW2096880157

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.