Evidence map›Paper›PMID 27757295›Full record

ArticleOncoimmunology

Cancer cell-derived IL-1α induces CCL22 and the recruitment of regulatory T cells.

Gabriela Maria Wiedemann, Max Martin Ludwig Knott, Viola Katharina Vetter, Moritz Rapp, Sascha Haubner, Julia Fesseler, Benjamin Kühnemuth, Patrick Layritz, Raffael Thaler, Stephan Kruger and 4 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

63 citing papers in PubMed, 99 citations in OpenAlex.

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3 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Gabriela Maria WiedemannCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Max Martin Ludwig KnottCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Viola Katharina VetterCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Moritz RappCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Sascha HaubnerCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Julia FesselerCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Benjamin KühnemuthCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Patrick LayritzCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
Raffael ThalerMedizinische Klinik und Poliklinik I, Klinikum der Universität München , Munich, Germany.
Stephan KrugerMedizinische Klinik und Poliklinik III, Klinikum der Universität München , Munich, Germany.
Steffen OrmannsDepartment of Pathology, Ludwig-Maximilians-Universität , Munich, Germany.
Doris MayrDepartment of Pathology, Ludwig-Maximilians-Universität , Munich, Germany.
Stefan EndresCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München , Munich, Germany.
David AnzCenter of Integrated Protein Science Munich (CIPS-M), Division of Clinical Pharmacology, Klinikum der Universität München, Munich, Germany; Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany.
Center for Integrated Protein Science Munich · DELMU Klinikum · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In cancer patients, immunosuppression through regulatory T cells (Treg) is a crucial component of tumor immune evasion and contributes to disease progression. Tumor-infiltrating Treg in particular suppress local effector T cell responses and are associated with poor prognosis in tumors such as human pancreatic cancer or hepatocellular carcinoma (HCC). The chemokine CCL22 is known to recruit Treg into the tumor tissue and many types of human tumors are known to express high levels of CCL22. The mechanisms leading to intratumoral secretion of CCL22 are so far unknown. We demonstrate here that intratumoral CCL22 is induced in tumor-infiltrating immune cells through cancer cell-derived interleukin-1 (IL-1α). In pancreatic cancer and HCC, CCL22 is produced by intratumoral dendritic cells, while the cancer cells themselves do not secrete CCL22

Indexed as

CCL22chemokineinterleukin-1regulatory T cellstumor

Identifiers

PMID27757295
PMCPMC5048775
OpenAlexW2343759513

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.