Evidence map›Paper›PMID 10587516›Full record

Trial reportThe Journal of clinical investigation1999

Interleukin-11 therapy selectively downregulates type I cytokine proinflammatory pathways in psoriasis lesions.

W L Trepicchio, M Ozawa, I B Walters, T Kikuchi, P Gilleaudeau, J L Bliss, U Schwertschlag, A J Dorner, J G Krueger

Erratum issuedOpen access · bronzeAbstract readClinical TrialClinical Trial, Phase I
In one paragraph

Trial report in The Journal of clinical investigation, 1999. 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 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 222 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

W L TrepicchioDepartment of Molecular Medicine, Genetics Institute, Cambridge, Massachusetts 01810, USA.
M Ozawa
I B Walters
T Kikuchi
P Gilleaudeau
J L Bliss
U Schwertschlag
A J Dorner
J G Krueger
Rockefeller University · USReproductive Genetics Institute · US

Funding

WOUND HEALING IN INDIVIDUALS OF DIFFERENT AGE AND GENETIC BACKGROUNDM01RR000102 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 1985 to 2006
$32.8M
CULTURED EPIDERMAL GRAFTS FOR BURN PATIENTSR01GM042461 · NIGMS · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI KATDARE, MEENA · 1989 to 2005
$1.4M
IMMUNOTHERAPY OF PSORIASIS--MECHANISM OF DAB 389R01AI039214 · NIAID · ROCKEFELLER UNIVERSITY · PI KRUEGER, JAMES G · 1996 to 2000
$375k
NCRR NIH HHS M01 RR000102NCRR NIH HHS MO1-RR-00102NIAID NIH HHS AI-39214NIGMS NIH HHS GM-42461NIGMS NIH HHS R01 GM042461
6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory skin disease in which epidermal hyperplasia results from skin infiltration by type I T lymphocytes and release of associated cytokines. A multifunctional cytokine, rhIL-11, modulates macrophage and type I T-lymphocyte function in cell culture and shows anti-inflammatory activity in animal models. We are testing subcutaneous delivery of rhIL-11 to patients with psoriasis in a phase 1 open-label dose-escalation clinical trial. Tissue was obtained from lesional and uninvolved skin before and during treatment with rhIL-11 and was examined by histology/immunohistochemistry and quantitative RT-PCR. Expression of over 35 genes was examined in all patients, and multiple genetic markers of psoriasis were identified. Expression of numerous proinflammatory genes was elevated in psoriatic tissue compared with nonlesional skin. Seven of 12 patients responded well to rhIL-11 treatment. Amelioration of disease by rhIL-11, as shown by reduced keratinocyte proliferation and cutaneous inflammation, was associated with decreased expression of products of disease-related genes, including K16, iNOS, IFN-gamma, IL-8, IL-12, TNF-alpha, IL-1beta, and CD8, and with increased expression of endogenous IL-11. We believe that this is the first study in humans to indicate that type I cytokines can be selectively suppressed by an exogenous immune-modifying therapy. The study highlights the utility of pharmacogenomic monitoring to track patient responsiveness and to elucidate anti-inflammatory mechanisms.

Indexed as

Antigens, SurfaceCytokinesDown-RegulationGene Expression RegulationGenetic MarkersHumansImmunohistochemistryInflammationInjections, SubcutaneousInterleukin-11KeratinocytesLeukocytesPsoriasisRecombinant ProteinsReverse Transcriptase Polymerase Chain ReactionRNA, MessengerAntigens, SurfaceCytokinesGenetic MarkersInterleukin-11Recombinant ProteinsRNA, Messenger

Identifiers

PMID10587516
PMCPMC409858
OpenAlexW1976494868

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.