Evidence map›Paper›PMID 9366578›Full record

ArticleThe Journal of clinical investigation1997

Interleukin-10 promotes activation-induced cell death of SLE lymphocytes mediated by Fas ligand.

L Georgescu, R K Vakkalanka, K B Elkon, M K Crow

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. 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
11.3field-weighted citation impact, top 1% 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, 178 citations in OpenAlex.

  1. Review
  2. Overview of Oxidative Stress in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023
    Review
  5. Review
  6. Clinical translation of immunomodulatory therapeutics.Advanced drug delivery reviews · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Monoclonal Antibodies for Systemic Lupus Erythematosus (SLE).Pharmaceuticals (Basel, Switzerland) · 2010
    Review
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 2 institutions in 1 country.

L GeorgescuSpecialized Center of Research (SCOR) in Systemic Lupus Erythematosus, Hospital for Special Surgery, New York, USA.
R K Vakkalanka
K B Elkon
M K Crow
Cornell University · USHospital for Special Surgery · US

Funding

SCOR IN SYSTEMIC LUPUS ERYTHEMATOSUSP50AR042588 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI CROW, MARY K · 1993 to 1997
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MOLECULAR ANALYSIS OF P/ANTIPR01AR038915 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI ELKON, KEITH B · 1988 to 1999
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NIAMS NIH HHS P50 AR42588NIAMS NIH HHS R01 AR38915
6 · The paper itself

Abstract

Immune function in SLE is paradoxically characterized by active T cell help for autoantibody production, along with impaired T cell proliferative and cytokine responses in vitro. To reconcile these observations, we investigated the possibility that the accelerated spontaneous cell death of SLE lymphocytes in vitro is caused by an activation-induced cell death process initiated in vivo. 27 SLE patients, three patients with systemic vasculitis, seven patients with arthritis, and 14 healthy subjects were studied. Patients with clinically active SLE or systemic vasculitis had accelerated spontaneous death of PBMC with features of apoptosis at day 5 of culture. A prominent role for IL-10 in the induction of apoptosis was observed, as neutralizing anti-IL-10 mAb markedly reduced cell death in the active SLE patients by 50%, from 22.3 +/- 5.2% to 11.2 +/- 2.8%, and the addition of IL-10 decreased viability in the active SLE group, but not in the control group, by 38%. In addition, apoptosis was shown to be actively induced through the Fas pathway. The potential clinical relevance of T cell apoptosis in active SLE is supported by the correlation of increased apoptosis and IL-10 levels in vitro with low lymphocyte counts in vivo. We conclude that the spontaneous cell death observed in vitro in lymphocytes from patients with SLE and other systemic autoimmune disorders results from in vivo T cell activation, is actively induced by IL-10 and Fas ligand, and reflects pathophysiologically important events in vivo. Activation-induced cell death in vivo provides a pathogenic link between the aberrant T helper cell activation and impaired T cell function that are characteristic features of the immune system of patients with SLE.

Indexed as

Lymphocyte ActivationAdultAntibodies, MonoclonalApoptosisArthritisArthritis, RheumatoidCD3 ComplexCells, CulturedCell SurvivalFas Ligand ProteinFemaleHumansInterleukin-10Interleukin-12Lupus Erythematosus, SystemicLymphocyte CountAntibodies, MonoclonalCD3 ComplexFASLG protein, humanFas Ligand ProteinInterleukin-10Interleukin-12Membrane Glycoproteins

Identifiers

PMID9366578
PMCPMC508464
OpenAlexW2020966657

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.