Evidence map›Paper›PMID 7500051›Full record

ArticleThe Journal of experimental medicine1995

Successful ultraviolet B treatment of psoriasis is accompanied by a reversal of keratinocyte pathology and by selective depletion of intraepidermal T cells.

J G Krueger, J T Wolfe, R T Nabeya, V P Vallat, P Gilleaudeau, N S Heftler, L M Austin, A B Gottlieb

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 249 citations in OpenAlex.

  1. Trial
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  9. Article
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  11. Article
  12. Immunotargeting in the management of psoriasis.ImmunoTargets and therapy · 2013
    Review
  13. Article
  14. Pruritus in cutaneous T-cell lymphoma: a review.Journal of the American Academy of Dermatology · 2012
    Review
  15. Light, including ultraviolet.Journal of autoimmunity · 2010
    Review
  16. Psoriasis assessment tools in clinical trials.Annals of the rheumatic diseases · 2005
    Review
  17. Review
  18. Immunopathogenic mechanisms in psoriasis.Clinical and experimental immunology · 2004
    Review
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

J G KruegerLaboratory for Investigative Dermatology, Rockefeller University, New York 10021, USA.
J T Wolfe
R T Nabeya
V P Vallat
P Gilleaudeau
N S Heftler
L M Austin
A B Gottlieb
Rockefeller University · US

Funding

WOUND HEALING IN INDIVIDUALS OF DIFFERENT AGE AND GENETIC BACKGROUNDM01RR000102 · NCRR · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY · 1985 to 2006
$32.8M
RESEARCH TRAINING IN DERMATOLOGYT32AR007525 · NIAMS · ROCKEFELLER UNIVERSITY · PI KRUEGER, JAMES G · 1986 to 1995
–
NCI NIH HHS CA-54215NCRR NIH HHS M01-RR00102NIAMS NIH HHS AR-07525
6 · The paper itself

Abstract

Skin irradiation with ultraviolet B (UVB) is a common and often durable treatment for psoriasis and other inflammatory skin disorders. We studied the effects of UVB on keratinocytes and leukocytes in psoriatic tissue and in culture. In nine patients treated repetitively, most of the cellular and molecular changes that typify the psoriatic epidermis reverted to normal. Keratinocyte hyperplasia, assessed by expression of the Ki-67 cell cycle antigen, decreased by 70%, and residual cell proliferation was appropriately confined to the basal layer. Epidermal thickening was reduced by 60%, and a granular layer reformed. Expression of keratin 16, as well as suprabasal integrin alpha 3 and insulin-like growth factor-1 receptors, was eliminated, whereas filagrin increased markedly. UVB also depleted > 90% of the CD3+, CD8+, and CD25+ T cells from the psoriatic epidermis, whereas dermal T cells were only minimally depressed. The latter finding parallels the known inability of these doses of UVB to penetrate the dermis. In tissue culture, UVB was antiproliferative and cytotoxic toward T cells and keratinocytes, but the T cells were 10-fold more sensitive. Furthermore, low doses of UVB induced apoptosis in lymphocytes but not keratinocytes, as detected by the TUNEL (TdT-mediated dUTP-biotin nick end labeling) technique. The selective effects of UVB on intraepidermal T cells in situ and in culture support the hypothesis that epidermal alterations in psoriasis can be normalized by a depletion of activated intraepidermal T cells.

Indexed as

Cells, CulturedDose-Response Relationship, ImmunologicEpidermisHumansIntercellular Adhesion Molecule-1KeratinocytesPsoriasisT-Lymphocyte SubsetsUltraviolet RaysIntercellular Adhesion Molecule-1

Identifiers

PMID7500051
PMCPMC2192269
OpenAlexW2117646004

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.