Evidence map›Paper›PMID 24226419›Full record

ArticleThe Journal of investigative dermatology2014

The role of IL-32 in cutaneous T-cell lymphoma.

Hiraku Suga, Makoto Sugaya, Tomomitsu Miyagaki, Makiko Kawaguchi, Hideki Fujita, Yoshihide Asano, Yayoi Tada, Takafumi Kadono, Shinichi Sato

Abstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.2field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  4. Review
  5. Article
  6. Review
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  8. Article
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  12. Article
  13. The Role of Tumor Microenvironment in the Pathogenesis of Sézary Syndrome.International journal of molecular sciences · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Interleukin 32 Promotes Foxp3Frontiers in cell and developmental biology · 2021
    Article
  18. Article
  19. Article
  20. 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

9 authors at 1 institution in 1 country.

Hiraku SugaDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Makoto SugayaDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan. Electronic address: sugayam-der@h.u-tokyo.ac.jp.
Tomomitsu MiyagakiDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Makiko KawaguchiDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Hideki FujitaDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Yoshihide AsanoDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Yayoi TadaDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Takafumi KadonoDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
Shinichi SatoDepartment of Dermatology, Faculty of Medicine, University of Tokyo, Tokyo, Japan.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-32 is a pro-inflammatory cytokine expressed by activated natural killer cells, T cells, keratinocytes, and fibroblasts. In this study, we examined the role of IL-32 in cutaneous T-cell lymphoma (CTCL), including mycosis fungoides (MF) and Sézary syndrome (SS). IL-32 mRNA expression levels in lesional skin of MF patch, plaque, and tumor were increased compared with those of normal skin, which positively correlated with CCL17 and CCL18 mRNA expression levels. Serum IL-32 levels positively correlated with disease activity within each patient. Immunostaining showed that keratinocytes expressed IL-32 in the lesional skin of MF patch and plaque, whereas in MF tumor, atypical T cells in the dermis strongly expressed IL-32. We also showed that IL-32 dose-dependently accelerated the proliferation of MF and SS cell lines in vitro, which was inhibited by blocking mitogen-activated protein kinase and NF-κB-mediated signaling. The addition of anti-IL-32 antibodies in culture decreased the proliferation of SS cells and the viability of MF cells, suggesting that IL-32 serves as an autocrine growth factor. In conclusion, our results suggest that IL-32 has a role in the formation and maintenance of CTCL lesions, providing a possible therapeutic target for patients with this disease.

Indexed as

AdultAgedCell Line, TumorCell ProliferationChemokine CCL17Chemokines, CCFemaleHumansInterleukinsLymphoma, T-Cell, CutaneousMaleMAP Kinase Signaling SystemMiddle AgedMycosis FungoidesNF-kappa BRNA, MessengerCCL17 protein, humanCCL18 protein, humanChemokine CCL17Chemokines, CCIL32 protein, humanInterleukinsNF-kappa BRNA, Messenger

Identifiers

PMID24226419
OpenAlexW1986553267

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.