Evidence map›Paper›PMID 39211051›Full record

ArticleFrontiers in immunology2024

IL-2 and TCR stimulation induce expression and secretion of IL-32β by human T cells.

Franziska Christine Sanna, Iva Benešová, Philip Pervan, Adriana Krenz, Alexander Wurzel, Robert Lohmayer, Jasmin Mühlbauer, Amélie Wöllner, Nina Köhl, Ayse Nur Menevse and 4 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. A single-cell cytokine dictionary of human peripheral blood.bioRxiv : the preprint server for biology · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. 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

14 authors.

Franziska Christine SannaInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Iva BenešováInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Philip PervanInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Adriana KrenzInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Alexander WurzelInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Robert LohmayerInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Jasmin MühlbauerInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Amélie WöllnerDepartment of Internal Medicine III, Hematology and Medical Oncology, University Medical Center, Regensburg, Germany.
Nina KöhlDepartment of Internal Medicine III, Hematology and Medical Oncology, University Medical Center, Regensburg, Germany.
Ayse Nur MenevseInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Slava StamovaInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Valentina VolpinInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Philipp BeckhoveInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.
Maria XydiaInterventional Immunology, Leibniz Institute for Immunotherapy, Regensburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-32 expression is important for pathogen clearance but detrimental in chronic inflammation, autoimmunity, and cancer. T cells are major IL-32 producers in these diseases and key mediators of pathogen and tumor elimination but also autoimmune destruction. However, their contribution to IL-32 biology during immune responses is hardly understood due to several isoforms with divergent inflammatory properties. Here, we identified IL-32β as the predominant isoform in various T cell subsets of healthy individuals and breast cancer patients with the highest levels detected in intratumoral regulatory T cells. We show that IL-32β is induced by IL-2 but IL-32β release requires T Cell Receptor rather than IL2R stimulation. Using inhibitors of protein secretion pathways and serial (ultra)centrifugation of T cell supernatants, we demonstrate that T cells actively secrete IL-32β unconventionally, as a free protein and, to a minor degree, through exosomes. Thus, our data identify activated T cells as major IL-32β secretors in health and cancer.

Indexed as

Breast NeoplasmsInterleukin-2InterleukinsLymphocyte ActivationReceptors, Antigen, T-CellFemaleHumansT-LymphocytesT-Lymphocyte SubsetsIL32 protein, humanInterleukin-2InterleukinsReceptors, Antigen, T-CellcancerexosomesIL-2IL-32 isoformIL-32 secretion mechanismIL-32βT cellsunconventional secretion pathway

Identifiers

PMID39211051
PMCPMC11357969

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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.