Evidence map›Paper›PMID 37409661›Full record

ArticleThe British journal of dermatology2023

Boost of innate immunity cytokines as biomarkers of response to extracorporeal photopheresis in patients with leukaemic cutaneous T-cell lymphoma.

Yi-Chien Tsai, Tanja Schlaepfer, Desislava Ignatova, Yun-Tsan Chang, Alan Valaperti, Boyko Amarov, Gabriela Blanchard, Kevin Pehr, Maya Vonow-Eisenring, Mirjana Urosevic-Maiwald and 7 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The British journal of dermatology, 2023. 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 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 7 institutions in 5 countries.

Yi-Chien TsaiDepartment of Dermatology, Lausanne University Hospital (CHUV), and Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Tanja SchlaepferDepartments of Dermatology.
Desislava IgnatovaDepartments of Dermatology.
Yun-Tsan ChangDepartment of Dermatology, Lausanne University Hospital (CHUV), and Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Alan ValapertiImmunology, University Hospital Zürich, Switzerland.
Boyko AmarovInstitute of Statistics and Econometrics, Faculty of Economics and Business Administration, Sofia University 'St Kliment Ohridski', Sofia, Bulgaria.
Gabriela BlanchardDepartment of Dermatology, Lausanne University Hospital (CHUV), and Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Kevin PehrDivision of Dermatology, McGill University, Jewish General Hospital, and Lady Davis Institute for Medical Research, Montreal, Canada.
Maya Vonow-EisenringImmunology, University Hospital Zürich, Switzerland.
Mirjana Urosevic-MaiwaldHautärzte-Zentrum am Zürisse, Zürich, Switzerland.
Wolfram HoetzeneckerDepartment of Dermatology, University Hospital Linz, Linz, Austria.
Steve PascoloDepartments of Dermatology.
Christoph IselinDepartment of Dermatology, Lausanne University Hospital (CHUV), and Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.
Christina FassnachtDepartments of Dermatology.
Florentia DimitriouDepartments of Dermatology.
Malgorzata BobrowiczDepartment of Immunology, Medical University of Warsaw, Warsaw, Poland.
Emmanuella GuenovaDepartment of Dermatology, Lausanne University Hospital (CHUV), and Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland.ORCID 0000-0001-5478-8735
University of Lausanne · CHUniversity Hospital of Zurich · CHImmunologie-Zentrum Zürich · CHJewish General Hospital · CAMedical University of Warsaw · PLSofia University "St. Kliment Ohridski" · BGWomen's General Hospital · AT

Funding

Swiss National Science Foundation IZLIZ3_200253
6 · The paper itself

Abstract

backgroundExtracorporeal photopheresis (ECP) has emerged as a systemic first-line immunomodulatory therapy in leukaemic cutaneous T-cell lymphoma (L-CTCL) and is now beginning to be utilized in other T-cell-mediated diseases. Although ECP has been used for nearly 30 years, its mechanisms of action are not sufficiently understood, and biomarkers for response are scarce.

objectivesWe aimed to investigate the immunomodulatory effects of ECP on cytokine secretion patterns in patients with L-CTCL, to help elucidate its mechanism of action.

methodsA total of 25 patients with L-CTCL and 15 healthy donors (HDs) were enrolled in this retrospective cohort study. Concentrations of 22 cytokines were simultaneously quantified by using multiplex bead-based immunoassays. Neoplastic cells in patients' blood were evaluated by flow cytometry.

resultsFirstly, we observed a distinct cytokine profile pattern difference between L-CTCLs and HDs. There was a significant loss of tumour necrosis factor (TNF)-α, and significant increase of interleukins (IL)-9, IL-12 and IL-13 in the sera of patients with L-CTCL compared with HDs. Secondly, patients with L-CTCL who received ECP were classified as treatment responders and nonresponders according to the quantitative reduction of malignant burden in their blood. We evaluated cytokine levels in culture supernatants from patients' peripheral blood mononuclear cells (PBMCs) at baseline and 27 weeks after ECP initiation. Strikingly, PBMCs purified from ECP responders released statistically higher concentrations of innate immune cytokines IL-1α, IL-1β, granulocyte-macrophage colony-stimulating factor (GM-CSF) and TNF-α in comparison with ECP nonresponders. In parallel, responders showed clearance of erythema, reduction of malignant clonal T cells in the blood, and a potent boost of relevant innate immune cytokines in individual patients with L-CTCL.

conclusionsTaken together, our results demonstrate that ECP stimulates the innate immune network, and facilitates redirection of the tumour-biased immunosuppressive microenvironment towards proactive antitumour immune responses. The alterations of IL-1α, IL-1β, GM-CSF and TNF-α can be used as biomarkers of response to ECP in patients with L-CTCL.

Indexed as

Lymphoma, T-Cell, CutaneousPhotopheresisSkin NeoplasmsBiomarkersCytokinesGranulocyte-Macrophage Colony-Stimulating FactorHumansImmunity, InnateLeukocytes, MononuclearRetrospective StudiesTumor MicroenvironmentTumor Necrosis Factor-alphaBiomarkersCytokinesGranulocyte-Macrophage Colony-Stimulating FactorTumor Necrosis Factor-alpha

Identifiers

PMID37409661
PMCPMC13077219
OpenAlexW4383293155

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.