Evidence map›Paper›PMID 8621796›Full record

ArticleThe Journal of clinical investigation1996

Hyperexpression of CD40 ligand by B and T cells in human lupus and its role in pathogenic autoantibody production.

A Desai-Mehta, L Lu, R Ramsey-Goldman, S K Datta

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed
7.7field-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

163 citing papers in PubMed, 521 citations in OpenAlex.

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  15. The role of soluble CD40L in autoimmune diseases.Journal of translational autoimmunity · 2025
    Review
  16. Article
  17. Review
  18. Review
  19. Mechanisms underlying sex differences in autoimmunity.The Journal of clinical investigation · 2024
    Review
  20. Article

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

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

4 authors at 3 institutions in 1 country.

A Desai-MehtaDepartment of Medicine, Northwestern University Medical School, Chicago, Illinois 60611, USA.
L Lu
R Ramsey-Goldman
S K Datta
University of Chicago · USCenter for Rheumatology · USNorthwestern University · US

Funding

MECHANISM OF AUTOIMMUNE RESPONSE IN HUMAN LUPUSR37AR039157 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DATTA, SYAMAL K · 2000 to 2009
$2.8M
SUPERANTIGEN INTERACTIONS WITH MHC CLASS II ANTIGENSP60AR030692 · NIAMS · NORTHWESTERN UNIVERSITY · PI POPE, RICHARD M. · 1986 to 2001
$2.1M
PATHOGENIC ANTIDNA AUTOANTIAB REGULATION IN LUPUSR01AR039157 · NIAMS · TUFTS MEDICAL CENTER · PI DATTA, SYAMAL K · 1989 to 1999
–
GENETIC-VIRAL-IMMUNOLOGIC STUDIES IN NEW ZEALAND MICER01CA031789 · NCI · TUFTS UNIVERSITY BOSTON · PI DATTA, SYAMAL K · 1985 to 1996
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NCI NIH HHS CA31789NIAMS NIH HHS AR30692NIAMS NIH HHS AR39157
6 · The paper itself

Abstract

We investigated the role of the costimulatory molecules, CD40 and its ligand CD40L, in the pathogenesis of human SLE. In comparison to normal subjects or patients in remission, PBMC from active lupus patients had a 21-fold increase in the frequency of CD40L-expressing, CD4+T cells. However, the expression of CD40L induced in either lupus or normal T cells by mitogenic stimulation could be down-regulated equally well by CD40 molecules on autologous B cells. Active lupus patients also had a 22-fold increase in percentage of CD8+ T cells expressing CD40L, consistent with their unusual helper activity in SLE. Surprisingly, patients with active lupus had a 20.5-fold increase in B cells that spontaneously expressed high levels of CD40L, as strongly as their T cells. Although lupus patients in remission had low levels of CD40L+ cells in the range of normal subjects, mitogen-induced upregulation of CD40L expression in the T and B cells was markedly greater than normal, suggesting an intrinsic defect. A mAb to CD40L blocked significantly the ability of lymphocytes from lupus patients with active and established disease to produce the pathogenic variety of antinuclear autoantibodies in vitro, bolstering the possibility of anti-CD40L immunotherapy for lupus. Future studies on the hyperexpression of CD40L could elucidate a regulatory defect in the pathogenic T and B cells of lupus.

Indexed as

AdolescentAdultAutoantibodiesBase SequenceB-LymphocytesCD40 AntigensCD40 LigandCD4-Positive T-LymphocytesCells, CulturedFemaleHumansLupus Erythematosus, SystemicLymphocyte ActivationMaleMembrane GlycoproteinsMiddle AgedAutoantibodiesCD40 AntigensCD40 LigandMembrane Glycoproteins

Identifiers

PMID8621796
PMCPMC507281
OpenAlexW2063661003

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.